ram.» . 3 . . v cum-u f... , , K ”gammy.“ .. . V ‘ . $3 1 ._ t in“ . .v. .2 .x r.- 7 {ME £ $3... .. u ...fiwhwwwux i... THESlS ZCCI This is to certify that the thesis entitled THE EFFECTS OF A HIGH-FIBER PRE-PUBERTAL FEEDING REGIMEN 0N IGF-l CONCENTRATION5, MAMMARY DEVELOPMENT, LACTATION POTENTIAL. AND REPRODUCTIVE PERFORMANCE IN SNINE presented by Pasha Ann Lyvers has been accepted towards fulfillment of the requirements for Master of Science degreein Animal Science (Ora W, @Véw Major professor Date July 6, 2000 MS U is an Affirmative Action/Equal Opportunity Institution LIBRARY Michigan State Unlverslty PLACE IN RETURN BOX to remove this checkout from your record. To AVOID FINES return on or before date due. MAY BE RECALLED with earlier due date if requested. DATE DUE [ DATE DUE DATE DUE "" -'[f.§__3’é 2091411 6/01 cJCIFlC/DateDuepss-p. 15 THE EFFECTS OF A HIGH—FIBER PRE-PUBERTAL FEEDING REGIMEN ON IGF-l CONCENTRATIONS. MAMMARY DEVELOPMENT. LACTATION POTENTIAL. AND REPRODUCTIVE PERFORMANCE IN SWINE BY Pasha Ann Lyvers A THESIS Submitted to Michigan State University In partial fulfillment of the requirements For the degree of MASTER OF SCIENCE Department of Animal Science 2000 ABSTRACT THE EFFECTS OF A HIGH—FIBER PRE-PUBERTAL FEEDING REGIMEN ON IGF—l CONCENTRATIONS. MAMMARY DEVELOPMENT. LACTATION POTENTIAL. AND REPRODUCTIVE PERFORMANCE IN SWINE BY Pasha Ann Lyvers Two hundred fifty-four crossbred gilts were allotted to a Moderate or Control nutrition regimen from 9 to 25 wk of age. The Moderate regimen alternated high-fiber (35% ground sunflower hulls) and low-fiber corn-soybean meal (CSBM) diets through four periods (one. two. three. and four). Control gilts were fed CSBM based diets in all periods. Ad-libitum access to feed was allowed with both regimens. After 25 wk of age. both treatment groups were managed similarly. Moderate gilt ADG was lower (P<0.01) during periods one and three. and greater (P=0.03) during period four. Concentrations of IGF—1 were lower (P<0.01) for Moderate gilts during period one and the first week of period three. however the high-fiber diet had no effect on IGF-l concentrations during the last week of period three. At puberty. age was similar; however. Moderates weighed less (P<0.01) than Controls. Analysis of mammary tissue collected on d 110 of gestation revealed Moderates had less (P<0.05) parenchymal tissue and tended to have less (P<0.10) mammary DNA when compared to Controls. However. during lactation Moderate females consumed more feed (<0.05). and tended to wean heavier (P<0.10) litters. TABLE OF CONTENTS LIST OF TABLES .................................... LIST OF FIGURES ...................... ............. INTRODUCTION ... ................................... CHAPTER 1 REVIEW OF LITERATURE ............................... Introduction .................................. Metabolsim of Fiber by Swine .................. Infleunce of dietary Fiber on Swine Performance and Behavior ................................. Growing Swine ............................ Sows ..................................... Digestibility of Different Fiber Sources ...... Milk Production in Swine ...................... Stages of Mammary Development ................ Embryonic and Fetal Development .......... Development of Mammary Gland from Birth to Conception ........................... Mammary Gland Development During Gestation Mammary Gland Development During Lactation Measurements of Mammary Development ...... ..... Hormonal Control of Mammary Development Role of Estrogen and Progesterone in Mammary Development ...................... Pubertal phase ..................... Gestation ........................... Prolactin ............................... Growth Hormone .......................... Effect of Insulin Like Growth Factor-1 (IGF-l) on Mammary Development ........... Placental Infleunces on Mammary Development ............................. Testosterone ........................... Nutritional Infleunces on Mammary Development and Milk Production ......................... Prior to Puberty Ruminants ......................... Non—ruminants ..................... Gestation ................................ Conclusion .................................. Literature Cited ............................ vii www 11 14 15 20 21 21 23 23 24 26 27 27 27 28 28 30 32 33 34 34 35 38 39 41 CHAPTER 2 THE EFFECTS OF A HIGH-FIBER PRE-PUBERTAL FEEDING REGIMEN ON IGF—l CONCENTRATIONS. MAMMARY DEVELOPMENT. LACTATION POTENTIAL. AND REPRODUCTIVE PERFORMANCE IN SWINE .......................................... Abstract ................................... Introduction ................................. Materals and Methods ......................... Experimental Design and Treatments ...... Animals .................................. Management ............................... Feed Analysis ................................. Blood Collection and Analysis ................. Mammary Tissue Collection and Analysis ........ Statistical Analysis .......................... Growth Performance ....................... Mammary Development ...................... Reproductive and Lactational Performance Results ....................................... Culling .................................. Growth Performance ....................... Plasma IGF-l ............................. Reproductive Development ................. Mammary Development ...................... Lactational Performance .................. Discussion .................................... Growth and Reproductive Performance ...... Culling Incidence ........................ Plasma IGF-l ............................. Mammary Development ...................... Litter Performance ....................... Implications .................................. APPENDICES APPENDIX A ......................................... APPENDIX B ......................................... APPENDIX C ......................................... iv 52 52 54 55 55 56 57 60 60 62 66 66 67 67 68 68 69 70 71 71 72 73 73 77 78 79 81 84 103 108 109 112 Table Table Table Table Table Table Table Table Table Table Table Table 10. 11. 12. LIST OF TABLES Diets fed during the four pre-pubertal feeding periods (Compositions of A. B. C. D. and E are shown in Table 3)... Composition of experimental grow-finish diets (as—fed basis) IIIIIIIIIIIIIIIIIII Composition of lactation diets (as—fed basis) .................................... Composition of diets fed from end of treatment periods through breeding and during gestation (as—fed basis) ........... Incidence of culling (from 9 wk of age to breeding for parity—two) as infleunced by pre—pubertal nutrition regimens ........ Growth performance of gilts reared using different nutritional regimens from 9 to 25 wk of age .............................. Effect of a pre-pubertal feeding regimen on weight. backfat depth (BF). loin-eye area (LEA). and age at puberty ............ Effect of a pre-pubertal feeding regimen on pre-lactational (d 110 of gestation) mammary development ....................... Effect of a pre—pubertal feeding regimen on sow backfat depth (BF) and loin—eye area (LEA) at breeding and farrowing. lactation feed intake (FI). lactation weight. backfat and loin-eye area change. and wean—to-estrus (WTE) interval ............................. Effect of a pre—pubertal feeding regimen On prolificacy in parity—one sows ........... Effect of a pre-pubertal feeding regimen on litter weights (kg) at d 0. 7. 14. and weaning ..................................... Effect of a pre—pubertal feeding regimen on litter gains (kg) between each weigh period at d 0 to 7. d 7 to 14. and d 14 to weaning ................................... 85 86 87 88 89 90 91 92 93 94 95 96 Table Table Table Table Table 13. 14. 15. 16 17. Composition of nursery diets ................. 105 Culling of early weaned gilts while in nursery .................................... 107 Plasma IGE-l concentrations (ng/mL) of gilts before and after dietary changes were Made through four different feeding periods .................................... 108 Effects of pre-pubertal feeding regimen and litter size on changes in sow weight. backfat (BE). loin—eye area (LEA). feed intake(FI). and wean-to-estrus (WTE) from farrowing to weaning ................................. 109 Effects of pre—pubertal feeding regimen and litter size on litter weights at d 7. 14. and weaning. and total litter gain between d 7 and weaning ................... 110 Figure Figure Figure Figure Figure LIST OF FIGURES Pre—pubertal feeding regimen and sampling time beginning at 9 wk of age and ending at 25 wk of age ......................... . The effects of a pre—pubertal feeding regimen on culling at different stages of development (*=P<0.05: **=P<0.01) ..... The effects of a pre-pubertal feeding regimen on locomotive and reproductive failure (*=P<0.01) ...................... . The effect of alternating a high—fiber diet with a corn soybean-meal diet on weight during four periods of growth. with the duration of the periods being 3. 3. 5. and 5 wk. respectively (means at the end of periods 1. 2. 3 and 4 were different at P<0.05) ..................... Changes in IGF-l concentration pre and post dietary changes during the experimental period. with weeks representing actual sampling time. and occurring 1 wk prior. and 1 wk post dietary changes. Diets were changed at end of wk 3. 6. 11. and 16 ..... 97 98 99 100 101 INTRODUCTION Sow milk production is important for the health and survival of the litter. Increasing sow milk production can improve litter growth. and increases in litter weaning weights can decrease days to market. Research has focused on improving sow milk production by altering hormone concentrations and nutrition during lactation (Farmer et al.. 1992; King et al.. 1993; Toner et al.. 1996) and gestation (Weldon. 1988: Howard. 1995). In heifers. milk production during first lactation improves when pre—pubertal energy intake decreases (Park et al.. 1987). This increase in milk yield is related to increases in pre-lactational mammary DNA and RNA. and growth hormone concentrations (Sejrsen. 1981). The increases in growth hormone associated with the decreased energy intake are thought to mediate mammary development via an IGF-l pathway. In swine. only two studies have examined pre-pubertal energy intake on milk production. Crenshaw (1990) saw a 36% increase in milk production when energy intake was restricted prior to puberty by the inclusion of fiber in the diet. and restricted during gestation by limiting feed intake. However. Sorensen and coworkers (1993) saw no improvement in milk production when restricting energy by limiting feed intake only during the pre—pubertal period. The objectives of this study were to evaluate the influence of a high-fiber diet fed intermittently during rearing. promoting periods of moderate and maximum growth. on mammary development on d 110 of gestation and parity—one lactation performance; and examine the IGF—l profile of pigs when fed high—fiber diets intermittently. By promoting periods of moderate and maximum growth during rearing. it is hypothesized that mammary DNA and RNA will be increased. This increase in mammary development will result in an increase in parity—one milk production. while the IGF—l profile will indicate how gilts respond to alternating periods of energy restriction. Chapter 1 REVIEW OF LITERATURE Introduction Initial research involving feeding fiber to swine explored the idea of using fiber as an energy source in order to reduce the amount of expensive high quality grains used in swine diets. However. use of fiber as an energy source is an inefficient biological process because fiber digestion occurs past the ileum. where far less nutrient absorption occurs. Due to reduced nutrient digestibility. reduced growth. and increased feed intake. feeding a high fiber diet is not recommended during the grow-finish period. when rapid growth is desirable. Although rapid growth is desirable for market swine. it has been proposed that growth of replacement gilts should be moderate. as restricting energy intake during rearing of gilts is beneficial in maximizing sow longevity (den Hartog. 1984). The benefits include prevention of excessive weight gain and back fat depth. and a decrease in number culled as a result of locomotive failure. Research to slow growth has often employed limit feeding. However. such dietary restriction often leaves pigs hungry. and increases stereotypic behavior (Hutson. 1989). Limiting feed intake also requires added feeding management. Gilts must be managed individually. and weighed periodically to determine prOper restriction of intake. Hence. fiber may be a beneficial feedstuff utilized in replacement gilt diets as a means of diluting energy and moderating growth. while providing gut fill to prevent hunger. and result in satiety. While it is known that adding fiber to swine diets restricts energy intake and decreases growth. it is not fully known what benefits fiber may have on sow performance. Research with heifers has shown that restricted energy during the pre-pubertal growth phase. occurring between seven and 10 mo of age. has resulted in greater milk production during the female’s first lactation (Sejrsen. 1981). The increase in milk production is thought to be a result of increased mammary development. and is mediated through changes in circulating hormones induced by limiting energy intake during rearing. Whether the same is true in swine is not known due to limited studies concerning pre- lactational mammary development and subsequent milk production. In sows. milk production is the major factor limiting pre-weaning growth rates. Approximately 95% of the piglets nutrient requirements are supplied by the sow's milk prior to weaning at 21 d (NRC. 1998). Maximizing the sow’s lactation potential can increase the number of pigs weaned per sow per year. and increase litter—weaning weights. The importance of the sow’s milk production for litter welfare warrants further research in the area of swine mammary development and milk production. Therefore. feeding a diet high in fiber to replacement gilts needs to be investigated further to determine if a pre-pubertal feeding regimen can maximize lactational performance. Metabolism of Fiber by Swine Dietary fiber is composed of four main constituents: cellulose. hemicellulose. pectins. and lignins. Located within the cell wall. these constituents provide tensile strength to the cell and contribute to plant structure. Cellulose. hemicellulose. and pectin are present in roughly equal amounts within the primary cell wall. and are of most concern when considering fibrous diets. The presence of these non-starch polysaccharides influences the digestion of fiber by different species (Calvert. 1991). Degradation of fiber across species is dependent on the enzymes in the stomach and intestine. Microbial organisms that produce cellulases. hemicellulases. pectinases. along with other enzymes are responsible for the degradation of fiber. In swine. these enzymes are found in greatest concentration in the cecum and colon. How these enzymes aid in fiber digestion depends on the source of fiber. along with the concentration of various minerals, vitamins, and nitrogen. which are essential for maintaining the microbial population (Varel and Yen. 1997). The enzymatic degradation of fiber can be measured by monitoring adenylate triphosphate (ATP) values throughout the gastrointestinal tract. When a diet high in fiber is fed there is an increase in ATP values. when compared to a low fiber diet. The increased ATP values represent the fermentation of carbohydrates from fiber and the accompanying release of energy by microorganisms. High ATP values have been seen throughout the stomach and gastrointestinal tract of pigs fed high fiber diets (Varel and Yen. 1997). When high fiber diets are fed. the release of ATP from fermentable carbohydrates further fuels microbial fermentation in the gastrointestinal tract. Thus. as fiber in the diet increases. the accompanying increase in ATP provides an energy source for microbial fermentation. therefore increased dietary fiber leads to increased microbial fermentation (Jensen and Jorgensen. 1994). It is within the large intestine and cecum that ATP values are the highest and microbial activity is the greatest. The microbial fermentation of fiber produces volatile fatty acids (VFA’s). mainly acetate. propionate. and butyrate (Rérat et al.. 1987). These VFA’s are rapidly absorbed and can provide up to 30% of the maintenance energy requirement for pigs (Yen et al.. 1991). However. VFA absorption by swine from digestion occurring post-ileum is less efficient than digestion occurring within or prior to the ileum. While fiber can contribute to the energy requirement. it depresses nutrient absorption in the small intestine (Dierick et al.. 1989). As mentioned previously. there is a reduction in nutrient digestion when fiber is added to the diet. This reduction in nutrient digestibility occurs mainly in amino acids and minerals (Eggum. 1995). This is hypothesized to be a result of: (1) an increase in wet digesta flow (2) erosion of the intestines mucosal surface as a result of higher digestive outputs of gastric. biliary. and pancreatic secretions (3) adhesion of the nutrients to the fiber particles. which leads to the nutrients being carried to the hind—gut. where they are not absorbed. but excreted (Jorgensen et al.. 1996). The changes in microbial activity associated with feeding fiber are dependent on the amount of fiber in the diet. Varel and Yen (1997) recorded that microbial activity was 5.5 times greater in pigs fed a high fiber diet. as compared to those on a low fiber diet. In the case of cellulolytic bacteria. no increase was seen in microbial activity when feeding a 20% corn-cob diet: however. a 200% increase was seen when diets containing 40-96% alfalfa meal were fed (Varel and Pond. 1985). This increase in microbial activity was not permanent. Once pigs were removed from the high fiber diet. cellulolytic bacteria numbers fell to the same number as pigs fed the standard diet. This suggests that although feeding fiber alters microbial activity. prolonged feeding of fiber is required for fiber degrading bacterial populations to be established and maintained in pigs (Anugwa et al.. 1989). Internal organ weight is affected by dietary fiber. An increase in empty weight of the small intestine. cecum. and colon occurs in young pigs fed high fiber diets (Kass et al.. 1980; and Pond et al.. 1989). In both experiments. 40% alfalfa meal was included in the diet. Pond and coworkers (1989) reported that the weights of the small and large intestine were increased when fiber was fed for 84 d. but stomach weights did not differ at that time. Anugwa and coworkers (1989) reported the relative weight of the stomach was significantly higher than the non-fiber fed controls after feeding a high fiber diet for 17 d. After 34 d of feeding a high-fiber diet there was an increase in cellulolytic bacteria numbers in the hind gut. but no difference in small and large intestinal weight between the control pigs. and those fed a high fiber diet. Within 32 d after being switched back to the control diet. stomach weight and cellulolytic bacteria numbers were similar for the control and high fiber diet pigs. Hence. the weights increase of portions of the gastro-intestinal tract appears to be dependent on duration of feeding the high fiber diet. The increased weight of the small and large intestine may require a longer duration of feeding a high fiber diet. Stomach weight increases relatively soon after a high fiber diet is fed. adapting to the high dietary fiber quickly. Influence of Dietary Fiber on Swine Performance and Behavior The utilization of fiber by the pig varies with the age of the animal. ambient temperature. fiber particle size. and fiber source (Nuzback et al.. 1984). The benefits of feeding fiber to swine have frequently been ignored because the addition of fibrous feeds in the diet decreases dry matter. energy. protein. and fiber digestibility when compared to swine fed a corn-SBM diet (Pollmann et al.. 1980: Calvert et al.. 1985). Growing'Sane Due to the growing pig’s inability to efficiently utilize dietary fiber. growth rate is often suppressed in young pigs fed a high—fiber diet as a result of the decreased daily energy intake (Kass et al.. 1980; Hale and Utely. 1985; Pond et al.. 1989). Depressed growth is not only a result of decreased energy intake. but also the decreased digestibility of amino acids and other nutrients. Apparent fecal digestibility of dry matter (DM) and crude protein (CP) are greater in pigs fed a low fiber diet. as compared to pigs on a high fiber diet (5.2% versus 9.2%. respectively). Inclusion rates as low as 5% fiber. with pectin (a water soluble component of the cell wall) as the fiber source. have resulted in lower fecal and ileal digestibility of several amino acids (den Hartog et al.. 1985). In contrast. Sauer and Hardin (1994) saw no differences on apparent ileal digestibility of amino acids. and no significant difference on DM digestibility when increasing the amount of fiber from 4.3% to 13.3%. The conflicting results between DM and amino acid digestibility may be a result of differing fiber sources. Oat husk meal and alfalfa meal were used as fiber sources by den Hartog and coworkers (1985). while Sauer and Hardin (1984) used solkafloc. Solkafloc is a purified fiber source consisting of 93% cellulose. while non—purified fiber of plant origin contains approximately equal amounts of cellulose. hemicellulose. and pectin. Pectin is a water-soluble fiber which reduces the mixing of intestinal contents. and blocks enzyme—substrate interactions. When pectin is included in the diet. a water layer may form around the ingesta. and prevent nutrient absorption (Sauer and Hardin. 1994). In young swine. the effects of fiber on digestion and growth vary depending on ambient temperature. When 10% alfalfa meal is added to the diet. daily gain is only depressed by 1% in a cold environment (10°C). However. in a warmer environment (35°C). daily gain is reduced by 5% (Stahly and Cromwell. 1986). This difference may result from an increase in basal heat production resulting from the inclusion of fiber in the diet. In the warmer environment. there is greater energy expenditure required to return the animals temperature to basal levels. and thus less energy devoted to animal growth. The effect of fiber on performance of growing pigs also varies with the duration of feeding the fibrous diet. Pigs fed fiber intermittently are as efficient at converting feed to gain as pigs fed a standard corn—SBM diet (Hale and Utely. 1985; Crenshaw. 1990). However. pigs switched from a low fiber to a high fiber diet do not increase feed intake 10 in order to sustain energy intake. and therefore growth is slowed (Hale and Utely. 1985). Pigs fed fiber continuously were significantly less efficient than phase~fed and control pigs. When pigs are fed a fibrous diet continuously. they compensate for the energy dilution effect of the fiber by increasing feed intake in order to sustain energy intake (Kennely and Aherne. 1980). Sbms The nutritional value of fibrous feeds is greater for sows than for growing pigs. The ability of sows to utilize fiber more efficiently is believed to be a result of increased size of the intestine. slower rate of passage of feed through the gastrointestinal tract. and larger microbial populations in the gastrointestinal tract (Nuzback et al.. 1984). Adult swine have up to 6.7 times more cellulolytic bacteria than growing animals. contributing to their greater utilization of fiber (Varel. 1987). Fiber is most commonly included in the diet of gestating sows in order to reduce constipation. However. various changes in reproductive performance have been noted as well. Piglet survival before weaning was higher in sows that ingest alfalfa meal (Pollmann et al.. 1980). or wheat shorts (Young and King. 1981) during gestation. The addition of straw meal (Munchow et al.. 1982) and wheat straw (Ewan et al.. 1996) has led to an improvement in the number of pigs born alive. Other research has shown no 11 significant differences in piglet survival. number born alive. or piglets weaned (Allee. 1976; Matte et al.. 1994; Vestergaard and Danielsen. 1998). Feeding fiber to gestating sows has also had negative reproductive effects. Fiber digestion by sows increases from early to mid gestation. however fiber digestion declines from mid gestation to late gestation (Calvert et al.. 1985). A decrease in fiber digestion in late gestation may result in a decrease in nutrient absorption and transport to the conceptus when demand for growth is the greatest. and could result in lower birth weights. As the percentage of alfalfa meal increases in gestation diets. piglet birth-weight decreases (Danielsen and Noonan. 1975; Calvert et al.. 1985). This has also been noted with the inclusion of 50% sugar beet pulp to the diet (Vestergaard and Danielsen. 1998). However. in the same experiment. a 50% fiber diet containing 15% grass—meal. 15% wheat bran. and 20% oat hulls did not affect piglet birth weight. During the trial. sows were fed similar levels of net energy. With the addition of grass-meal. wheat bran. and oat hulls to the gestation diet. sow feed intake increased. With the sugar beet pulp diet sows did not increase feed intake and therefore. there was a reduction in net energy intake. These differences between dietary energy intake contribute to the conflicting results in litter birth weights. and reveal how different dietary fiber sources can elicit different responses on animal performance. 12 Feeding fiber to gestating sows can also potentially impact sow behavior. A diet with 97% alfalfa hay results in sows being more docile and easier to manage than sows that did not ingest alfalfa hay (Danielsen and Noonan. 1975). Sows that received a diet containing both wheat bran (41%) and corn cobs (53%). or a diet containing both oat hulls (53%) and oats (41%) show less repetitious behavior and spend more time resting than sows fed a corn soybean meal diet (Matte et al.. 1994). In addition. there is a 12.8% increase in resting time for parity—one sows receiving a wheat bran and corncob diet. During parity-two there is a 50% decrease in stereotypic behavior (head waving. horizontal head movements. and bar biting) for sows fed high-fiber (94%) during gestation (Robert et al.. 1993). This change in behavior represents a 10% reduction in energy used for maintenance. Therefore. more energy can be directed toward body weight gain (Noblet et al.. 1989). A reduction in aggression and sham chewing was observed for sows housed in individual stalls fed sugar beet pulp; however. in the same experiment. sows fed a fibrous diet containing grass—meal. wheat bran. and oat hulls showed no change in behavior (Vestergaard and Danielsen. 1998). The sugar beet pulp diet caused a longer lasting rise in insulin and glucose than did the control diet. and the fibrous diet containing grass—meal. wheat. and oat hulls. This extended rise indicated a prolonged satiety when the sugar beet pulp diet was fed (Vestergaard and Danielsen. 1998). 13 Digestibility of Different Fiber Sources The overall outcome achieved when feeding fiber to swine may vary with fiber source. as a result of the differences in fiber digestibility as influenced by individual fiber components. Crude fiber can be digested with a neutral detergent to separate fiber into cell contents and cell wall components. The cell wall components (cellulose. hemicellulose. and lignin) are referred to as neutral detergent fiber (NDF) and are water insoluble (Van Soest. 1967). The water soluble cell contents include sugars. starches. pectins. proteins. lipids. and vitamins. An increase in NDF intake results in a decrease in dry matter (DM). nitrogen. and energy digestibilities (Stanogias and Pearce. 1985). The inclusion of NDF in the diet increases the rate of DM flow (g/d). When comparing NDF from different fiber sources (purified NDF. wheat bran. or sunflower hulls). rate of DM flow is more dependent on level of NDF in the diet than the source of NDF (Schulze et al.. 1995). However. the amount (g/kg of DM intake) of total nitrogen passing through the terminal ileum is influenced by both NDF concentration and source. An explanation for this occurrence may be the result of fiber composition within the NDF fraction of these fiber sources. Although wheat bran and purified NDF (from wheat bran) have similar insoluble 14 fiber profiles. the water-soluble portion of purified NDF may be more similar to that of the sunflower hulls diet resulting in similar nitrogen flow. Pectins were removed in the process of developing the purified NDF. However. pectins were not removed from the wheat bran or sunflower hull diets. As stated previously. the gelling and viscosity of water-soluble fibers such as pectins reduces the mixing of intestinal contents. and blocks enzyme-substrate interactions. A water layer may form around the ingesta. and prevent nutrient absorption (Sauer and Hardin. 1994). Therefore. if the level of pectin in sunflower hulls is low. this could account for the similar N flow observed between the purified NDF and sunflower hulls. Due to the differences in nutrient digestibility between different sources of dietary fiber. caution should be taken when including fiber in swine diets. Limited knowledge of nutrient availability from fiber sources. and the reduction in energy. amino acid. mineral. and vitamin absorption when fiber is added to the diet may result in imprecise diet formulations. This could lead to detrimental effects on growth and performance. Milk Production in Swine Fiber is not typically fed during lactation as the sow‘s milk contributes to the health. survivability. and growth of the nursing pig. It is important that energy 15 intake not be reduced by the addition of fiber to lactating diets. so that milk production can be maximized. Milk production is important in increasing the survivability of pigs to be weaned per sow per year. and increasing litter— weaning weights. It is not uncommon for producers to lose between 10 to 25% of pigs farrowed before they are weaned. Starvation is a contributing factor to pre-weaning mortality. Furthermore. an increase in litter weaning weights affects lifetime market hog growth performance. including days to market (Mahan and Lepine. 1991). The sow’s milk is the major nutrient source for the pig prior to weaning. When creep feed is offered during the first three weeks. only 5% of the piglet’s nutrient requirements are met. Therefore. the sow’s milk supplies approximately 95% of the nutrient needs of the piglet prior to 21 days of age. Between the third and fourth week of lactation. growth rate of the piglet surpasses milk production of the sow. and the sow's milk can no longer meet the piglet’s nutrient needs (Hartman et al.. 1984). Therefore. it has become a common practice to wean pigs at about 21 days of age. Energy is one of the major nutrient requirements of the newborn pig and is supplied from milk lipids and sugars. The major milk sugar is lactose. Lactase. the enzyme that hydrolyzes lactose to glucose. is highly active at birth. while amylase. which hydrolyzes cornstarch. is absent (Pekas. 1991). As the pig matures lactase will decrease. 16 while amylase increases. allowing for the digestion of vegetable-based diets. The sow’s mammary gland contains no gland cistern to store milk: therefore. milk cannot be withdrawn through the teats via suckling. The milk ejection reflex in swine is dependent on a neuro—endocrine pathway. which involves the release of oxytocin and the ejection of milk (Lincoln and Paisley. 1982). The release of oxytocin from the posterior pituitary gland is initiated through the stimulation of neural receptors located within the teats of the mammary gland. Suckling by piglets is the stimuli for these receptors. On average. piglets suckle 20 times or more a day (Fraser. 1980) at intervals of 44.3 minutes with a range of 21 to 92 minutes (Ellendorf et al.. 1982). Piglets allowed to suckle every two to three hours consume less milk than those allowed to suckle every hour (Barber et al.. 1955). Conversely. when nursing intervals are controlled at 35 min as compared to 70 min. piglets consumed less milk per nursing bout at the shorter intervals. Despite this. piglets suckling at shorter intervals consumed overall 27% more milk and gained 44% more weight. When nursing frequency is shortened the occurrence of incomplete suckling. or suckling without milk injection increases (Spinka et al.. 1997). Approximately 21.4% of sucklings are unsuccessful (Ellendorf et al.. 1982). It is unknown whether these incomplete or unsuccessful nursings are 17 detrimental to the sow‘s milk ejection reflex and piglet growth. There is a direct correlation between litter size and milk production (King et al.. 1989). When litter size is increased. milk yield increases. This linear relationship was not as strong in late lactation when milk output approached its maximum potential (Auldist et al.. 1998). Despite increased total milk production. individual pig growth rate decreased linearly with increased litter size. During late lactation growth rate decreased from 309 g/day to 199 g/day when litter size increased from six to 14 piglets (Auldist et al.. 1998). Although. suckling intervals were similar between litter sizes during late lactation. larger litters suckled more frequently during early lactation. Because there is no milk storage prior to ejection. measurements of milk yield are often difficult in swine. Weigh-suckle-weigh. isotope dilution. machine milking. and weekly piglet weights have all been used as methods for determining a sow’s milk yield. Weigh-suckle-weigh and isotope dilution are the two most commonly used methods. Weigh-suckle—weigh involves the weighing of individual piglets before and after a suckling interval. A correction factor is often used to account for metabolic changes that may occur between weighings (Klaver et al.. 1981). This method often underestimates milk yield. and is subject to error if the piglet urinates or defecates between nursing 18 and weighing. Milk yield may be compromised because the piglets are not allowed to nurse naturally. and nursing intervals are predetermined by the researcher (Pettigrew et al.. 1985). Isotope dilution is considered the most accurate of the methods because it does not disrupt natural suckling intervals. It involves the use of a hydrogen isotope (IND) as a tracer to estimate body water turnover. and assumes milk is the only source of water to the piglet. After piglets are fasted to standardize gut fill. they are injected with D20 according to body weight. Piglets are fasted a second time after injection to equilibraterILO with body water. Piglets are then returned to the sow for the measurement period. after which they are fasted and a second blood sample is taken. There is a second Dfi>injection. followed by a third blood sample. Based on the composition of milk. the amount of milk consumed can be determined from the blood samples (Pettigrew et al.. 1985). Machine milking of sows is accompanied with injections of oxytocin to allow milk ejection (Hartmann and Pond. 1960). Like weigh-suckle- weigh. it does not allow for the natural release of milk through suckling intervals. and often sows must be restrained. Disturbance to the sow may decrease milk yield. Lewis and coworkers (1978) estimated sow milk production with weekly weighings of individual piglets. This method requires that genetics and environmental conditions be controlled. in addition to litter size. lactation length. and piglet weight at birth. 19 Stages of Mammary Development Improving milk production in the sow requires an understanding of the mammary gland. and factors (such as hormones and nutrition) which effect mammary gland development. Anatomically the sow differs from many mammalian species in that the mammary gland location is abdominal versus inguinal. The sow has four to nine pairs of mammary glands located on either side of the midline along the entire abdominal wall. Like other mammals. the sow’s mammary gland consists of parenchymal. and extraparenchymal tissue. Each gland consists of a teat with two streak canals per teat. The streak canal opens into a very small teat cistern. and allows the removal of milk through the teat. The teat cistern of sows differs from ruminants in that it is not large enough to allow for storage of milk prior to suckling. The teat cistern is further connected to a gland cistern. A network of ducts is located above the gland cistern. and branch through all areas of the stroma. The stroma supports and protects the parenchyma. and in a fully developed gland. divides it into lobes and lobules located at ductal extremities (Cowie and Tindal. 1971). Within each lobule are 150 to 225 alveoli (Bearden and Fuquay. 1992). The alveoli are tiny sac like structures enclosing a lumen lined with epithelial cells. 20 The epithelial cells are the basic secretory unit of the mammary gland. Over half of the milk stored in a mammary gland will be stored in the lumen. In the sow. secretory activity of the alveoli is minimal until 2 days prior to parturition (Anderson et al.. 1985). Ebbryonjc ana’fbtaj.flevajqpmant In many domestic species. prenatal development of the mammary gland occurs in a similar sequence. The mammary gland develops in a discontinuous manner during five distinct periods: fetal. pre—pubertal. post—pubertal. gestational. and early lactation (Oka et al.. 1991). The mammary gland begins to develop early in the embryonic stage beginning with the formation of the mammary band. Mammary band growth is then followed by a rapid succession of stages known as the streak. line. crest. hillock. and bud. With the development of the bud occurring as the embryo becomes a fetus. During the fetal stage. primary. secondary. and possibly even tertiary. spouts will form. These spouts are the initial stages of the milk secretion tissue (Bearden and Fuquay. 1992). .09 V91 oping/2 t 0f the Mammary 6'1 and from 312‘ t!) to Can cap no” The mammary gland is unique from other organs in that it is immature at birth. Following birth. the mammary gland consists of immature ductlar and secretory alveolar epithelial cells known as the parenchyma. The parenchyma is 21 located in a matrix of other cell types including myoepithelial cells. adipocytes. fibroblasts. and smooth muscle which make up the stromal portion of the mammary gland (Tucker. 1987). After birth. the mammary gland grows at a rate proportionately equal to body growth. or isometrically. Prior to the onset of puberty. the mammary gland grows at a rate faster than the rest of the body. In heifers this increased growth phase begins around three months of age. and in rats it begins around 30 d of age (Tucker. 1987). In heifers. growth rate of the mammary gland is 3.5 times faster than the growth rate of the body (Bearden and Fuquay. 1992). At this time. the ducts will elongate into the stromal portion of the mammary gland. The stroma will also increase with the elongation of the ducts (Reece. 1958). This growth of mammary ductal tissue into the fat pad is defined as the allometric growth phase. In rats and heifers. the allometric growth continues through several estrous cycles and then returns to isometric rates until conception (Tucker. 1969; Sinha and Tucker. 1969a). Regulation of the isometric and allometric growth phases is related to the secretory patterns of estradiol and progesterone. In general. estradiol and progesterone secretion is asynchronous during the estrous cycle. whereas during pregnancy both hormones increase simultaneously (Britt et al.. 1981). Within an estrous cycle most of the increase in mammary gland development occurs near estrus. 22 while mammary gland development is generally slowed during the luteal phase of the estrous cycle. which may account for the failure of the mammary gland to maintain allometric growth prior to conception (Sinha and Tucker. 1969a: Sinha and Tucker. 1969b). .mammary'GYandflDevejqpmant.DUrjag'Gastatjon At conception. mammary ducts begin to proliferate further into the mammary fat pad and the true alveoli form and begin to replace lipid in the mammary fat pad (Tucker. 1969). In mice. the size of the fat pad can become a limiting factor in parenchymal growth (Hoshino. 1964). During the initial stages of pregnancy little development of the mammary gland occurs. However. during the final stages of gestation the mammary gland undergoes a second allometric growth phase(Hacker and Hill. 1972; Tucker. 1987). In swine. this allometric growth occurs during d 50 and d 100 of gestation. with a massive proliferation of mammary cells (Hacker and Hill. 1972). During this last stage of gestation. the development of uterine and placental tissue is complete. and estrogen output from the uterus increases. which may be responsible for the allometric growth experienced during late gestation (Knight et al.. 1977). Mammary 6'1 and 09 V91 apple/2 t During Lacta £101) Mammary tissue does not express its maximum potential for development until lactation. when the gland switches 23 from a nondifferentiated to differentiated state and begins synthesizing and secreting milk (Oka et al.. 1991). There is a high correlation (r = .85) between milk yield at first lactation and mammary cell number in rats (Tucker. 1966). Therefore. mammary epithelial cell numbers are often used as a major determinant of milk yield. As mammary cell numbers in rats decreases. so does milk yield (Tucker. 1987). In rats. an increase in mammary cell number during lactation is observed as suckling stimuli increases (Tucker et al.. 1967). In swine. milk yield is shown to increase with increases in litter size as a result of increased suckling stimuli (Toner et al.. 1996). As with rats. this increase in milk production as a result of suckling stimuli may be related to mammary cell number. Recent research has indicated that the mammary gland in swine continues to grow from d 0 to d 21 of lactation. and is influenced by litter size (Kim et al.. 1999). Suckling intensity also increases blood flow to the mammary gland. which may aide in adjusting milk yields to meet the needs of the young (Tucker. 1981). Measurements of Mammary Development In 1953. Kirkham and Turner first reported the use of deoxyribonucleic acid (DNA) as an estimate of secretory tissue (mammary epithelial cell number). The DNA content per mammary cell nucleus is constant during pregnancy and lactation (Tucker. 1987). and therefore. can give an 24 indication of the number of secretory cells present. However. changes in total mammary DNA do not necessarily reflect changes in numbers of secretory cells (Tucker. 1981). because DNA is contained in other cell types within the mammary gland including adipocytes and fibroblasts (Weldon. 1988). Ribonucleic acid (RNA) is a reflection of the functional state of the cell and represents cell secretory activity. The RNA/DNA ratio can be used as a measure of protein synthesis activity per cell in the mammary gland (Howard. 1995). An increase in the RNA/DNA ratio represents the transition between a non-lactating state to a lactating state. In the rat. pre—lactational mammary gland total DNA (r = .85) and RNA (r = .93) is highly correlated with litter weight gains (Tucker. 1969). Thus. DNA and RNA of mammary gland tissue is used to estimate subsequent milk production. In swine. DNA and RNA measurements have been used to study pubertal and gestational development of the mammary gland. In 1972. Hacker and Hill examined mammary development in virgin and pregnant swine. Results indicate that DNA and RNA remain unchanged between gilts in estrus compared to gilts at 25 days and 50 days of pregnancy. However. between day 50 and day 100 of gestation. DNA and RNA increased 5.0 and 7.5 times. respectively. With an increase in DNA and RNA. a decrease in lipid content of the mammary gland is observed. In 1982. Kensinger and coworkers performed a similar trial. At 30 d of gestation until 75 d. the mammary gland of swine. as measured by dry fat free tissue (DEFT) and DNA. grew at a fairly constant rate. After 75 d the growth rate of the mammary gland began to increase steadily. until the growth rate of the mammary gland was approximately four times that of the total mammary growth prior to 75 d. Dry fat free tissue and DNA followed similar patterns of increase throughout gestation. indicating that the lipid portion of the mammary gland began to decrease as the parenchymal and stromal portions extended into the fat pad. Hormonal Control of Mammary Development Hormones are the primary physiological factors that stimulate mammary growth. and initiate and maintain milk production. Ovariectomies performed on rats inhibited mammary development. indicating that hormones produced by the ovaries play a role in mammary development. The ovary releases both estrogens and progestins. while the anterior pituitary gland secretes growth hormones and prolactin. During the later part of gestation. the placenta provides a source of estrogen and progesterone in swine. In many species the placenta is also a source of placental lactogen. a hormone which shares similarities with growth hormone and prolactin to promote mammary growth (Anderson et al.. 1985). 26 ija of Estrogen anafiRquasterona In mammary Davejqpmant .PUbartaJ phase. ZEstrogen’s main role in mammary development is ductal growth. therefore it is at pro-estrus that a surge in ductal growth occurs due to increasing estrogen concentrations. During the estrous cycle. the majority of mammary development occurs prior to estrus. when estrogen concentrations are greatest. Limited mammary development occurs during the luteal phase. when progesterone concentrations are elevated. Therefore. once puberty begins. the asynchronous regulation of estrogen and progesterone concentrations limit mammary growth (Sinha and Tucker. 1966: Sinha and Tucker. 1969b). (fiestatjon. IProgesterone is at greatest concentrations during the luteal phase (when corpora lutea are present). and has the greatest influence on mammary development during gestation. Progesterone inhibits lactogenesis. and influences proliferation of lobule-alveolar secretory tissue. Due to the corpus luteum. progesterone concentrations are maintained during gestation. Prior to complete regression of the corpus luteum. estrogen concentrations increase approaching parturition. While the pre—pubertal allometric growth phase is inhibited by progesterone. the increasing progesterone and estrogen concentrations. seen during gestation. initiate the second allometric growth phase. and a surge in mammary development. The amount of mammary growth that occurs during gestation is dependent on the species. In rats. 60% of mammary growth 27 occurs during gestation. while 94% of total mammary growth occurs during gestation in the hamster. (Tucker, 1969; Knight and Peaker. 1982). Pro] a 5‘ tin Despite estrogen and progesterone's role in mammary development. both hormones were ineffective in stimulating mammary growth in hypophysectomized animals implying the importance of pituitary hormones (Turner. 1970). Prolactin along with growth hormone restores mammary atrophy caused by hypophysectomies (Anderson et al.. 1985). A small increase in prolactin is seen at pro—estrus. however during pregnancy prolactin remains at basal concentrations because it is inhibited under the presence of progesterone. Therefore. prolactin only acts on the first allometric growth phase. Prolactin is needed for optimal lobule-alveolar development but is not limiting to the mammogenic process. Its main effect is exerted at the onset of lactation. Although several hormones are needed for lactation. prolactin is the major hormone required for milk secretion in many species. including swine. GTowtn hbnmona There is a strong positive correlation between growth hormone and mammogenesis between birth and conception (Tucker. 1987). Pre-pubertal administration of growth hormone has resulted in an increase in the amount of 28 parenchymal tissue in heifers (Sejrsen et al.. 1986). In sheep. growth hormone concentrations have been shown to be positively correlated with the amount of parenchymal tissue within the mammary gland (Johnsson et al.. 1986). In rats and heifers. growth hormone primarily stimulates ductal development. but it works in conjunction with prolactin. estrogen. and progesterone to stimulate a marked increase in lobule-alveolar growth. A decrease in mammary growth is associated with lower concentrations of growth hormone. In heifers. stimulating the secretion of growth hormone leads to increased milk yields (Tucker. 1981). Growth hormone may also increase milk yield during lactation by increasing cardiac output to the mammary gland (Hanwell and Linzell. 1973). A relationship between growth hormone and nutrition has been established in sheep and cattle. An increased plane of nutrition during the first allometric growth phase results in a decrease in growth hormone concentrations. However. this decrease is only noted prior to puberty. Growth hormone concentrations were significantly lower in heifers on a high plane of energy versus heifers fed restricted energy before puberty. but not after puberty (Sejrsen et al.. 1983). Pre—pubertal lambs fed restricted diets had greater mean plasma concentrations of growth hormone and decreased concentrations of prolactin. These results coincide with an increase in mammary development. The effect of nutrition on mammary development decreased as the 29 lamb’s age increased (Johnsson et al.. 1986). The failure of the mammary gland to maintain allometric growth is hypothesized to be a result of the differences in growth hormone concentrations seen before and after puberty. In swine. limited studies have been conducted evaluating the administration of growth hormone to improve mammary development. Howard (1995) observed an increase in parenchymal tissue. DNA. and RNA with the administration of growth hormone during late gestation (91 d). However. subsequent milk production was not measured. .Effact of Insulin Like Growth factor-J {16?11/ 0n.Mammany .vaajqpment Currently. there is no evidence to indicate that growth hormone can bind to mammary tissue. Thus. it has been speculated that growth hormone acts indirectly on the mammary gland via IGF-l (Sejrsen. 1994). In vitro. IGF-l binds to receptors on the surface of epithelial cells located on the mammary gland. initiating the tyrosine phosphorylation pathway. resulting in the stimulation of DNA synthesis of bovine mammary tissue (Oka et al.. 1991). In swine. hypophysectomies to suppress release of growth hormone also suppresses IGF-l concentrations. and administration of growth hormone to normal and hypophysectomized pigs increases IGF-1 (Buonomo et al.. 1987: Armstrong et al.. 1989). Insulin like growth factor— 1 concentrations increased four to six hours after growth 30 hormone injections. and IGF—1 concentrations remained elevated for up to 24 h after growth hormone concentrations returned to normal. This indicates that growth hormone induces synthesis of IGF-1. rather than causing it’s release from storage pools (Sillence and Etherton. 1986). In 1990. Owens and coworkers saw that treatment of pigs with growth hormone led to significant increases in IGF-l concentrations. On the other hand. a second study by Owens and coworkers (1991) saw no relationship between endogenous growth hormone and IGF-1. Growth hormone pulses from the anterior pituitary gland were not accompanied with distinguishable changes in plasma IGF-l. Plasma levels of growth hormone in weaned. pre—pubertal pigs are low compared with other species at similar stages of postnatal development (Owens et al.. 1991). This may have contributed to the observation that endogenous growth hormone and IGF—1 did not exhibit the relationship that has been seen in other species. According to Owens and coworkers (1991). swine growth hormone regulation of IGF—1 may be dependent on growth hormone exceeding normal physiological concentrations. In heifers (Capuco et al.. 1995). and swine (Rozeboom. 1992) restricted energy intake decreases IGF-l concentrations. This goes against previous assumptions that implicate a growth hormone/IGF—l pathway in nutritionally mediated mammary development. Research has indicated that the growth hormone/IGF—l axis becomes uncoupled when animals 31 are fed a restricted energy intake. and as growth hormone increases. IGF—l decreases (McGuire et al.. 1992). With the uncoupling of the growth hormone/IGF-l axis. the role of IGF-1 in mammary development during periods of energy restriction is uncertain. PVacantaJ Influences on mammary Davajqpmant During early pregnancy. maternal hormones are responsible for mammary growth. Hypophysectomies after mid pregnancy do not affect mammary cell number. suggesting that the placenta supplies a source of hormones needed for mammogenesis (Leonard. 1945; Pencharz and Long. 1933). In swine. the placenta is a source of estrogen and progesterone. An increase in mammary tissue growth between 75 d and 90 d coincides with the completion of placental growth (Knight et al.. 1977). A positive correlation between mammary development and the number of fetuses and weight of the placenta of litter- bearing species exists. An increase in mammary development is believed to be a direct result of an increase in placental lactogen associated with increased placenta size (Hayden et al.. 1979). In pregnant rats and mice. as the number of fetuses increase. the concentration of placental lactogen also increases. Although unique to the placenta. placental lactogen is structurally similar and can replace prolactin and growth hormone. In sheep and goats. the most intense growth of the lobule—alveolar tissue occurs when 32 placental lactogen secretions are at their greatest. In cattle the role of placental lactogen is unclear. In most species that secrete placental lactogen. placental lactogen is released into maternal circulation. where it can bind to prolactin receptors to stimulate mammary growth. In cattle. placental lactogen is secreted primarily into fetal circulation (Anderson et al.. 1985). In swine lactogenic activity from.placental extracts has not been detected. therefore. it is unknown how fetal number affects mammary development. However. because the placenta is a source of estrogen and progesterone. fetal number and placenta size may influence swine mammary development through these hormones (Knight and Peaker. 1982). Iastastarana Embryonic mammary development is similar for both the female and male. During fetal development mammary growth differentiates between the two sexes. Testosterone injections in pregnant mice lead to the death of cells surrounding the epidermal cone. thus resulting in no formation of mammary tissue associated with milk production (Andersen et al.. 1985). Similar results were seen in rats and horses. Testosterone is therefore considered responsible for reduced epithelial tissue common in male mammary glands. 33 Nutritional Influences on Mammary Development and Milk Production Prior to puberty .RUmjnantsz Changing dietary energy levels leads to a change in relative amounts of parenchymal and extraparenchymal tissue in heifers (Sorensen et al.. 1964: Sejrsen et al.. 1982: Stelwagen and Grieve. 1989). In dairy heifers (Swanson. 1960: Little and Harrison. 1979). beef heifers (Ferrel. 1982. Hixon et al.. 1982). and sheep (Johnsson and Hart. 1985: Johnsson et al. 1986). a high plane of nutrition prior to puberty decreases milk yields during lactation. However. when placed on a restricted diet prior to puberty. milk yield increases. Therefore. a high plane of nutrition during the allometric growth phase of the mammary gland is assumed to limit mammary development. The detrimental effects of a high plane of nutrition on subsequent milk production have been attributed to a reduction in parenchymal tissue. Parenchymal tissue is most sensitive to high planes of nutrition during pre-pubertal development when the mammary gland is undergoing the allometric growth phase (Carstens et al.. 1997). In cattle. restricted feeding. when compared to ad— libitum feeding during the pre-pubertal phase. increases mammary secretory tissue weights by 23% and DNA content by 32%. Although restricted feeding offers promising mammary growth results. it also may lead to a delay in age at first estrus (Sejrsen. 1981). To obtain desired results in both mammary development and age at puberty. a restricted- compensatory feeding regimen has been tested. Dairy heifers fed alternating periods of restricted and compensatory energy intake produced 16% more milk during a 250 d lactation (Peri et al.. 1993). In a more recent study. restricted-compensatory crossbred heifers produced 39% more milk by 30—d post-partum and weaned 11% heavier calves. In both experiments. the age at puberty was not significantly different between treatments (Carstens et al.. 1997). Despite the detrimental effects a high plane of energy exhibits on milk production when fed during the pre-pubertal phase. no negative effects of feeding an increased level of energy on mammary development during the post-pubertal stage has been observed in cattle (Sejrsen et al.. 1980). This may be due to mammary growth returning to isometric growth rates after puberty. Aha-ruminants: In rats. mammary development occurs in a similar pattern as what has been observed in heifers. Increased energy intake during the first allometric phase leads to decreased mammary parenchymal tissue. and decreased subsequent milk yields (Sinha and Tucker. 1969). In swine. most nutrition research to improve mammary development has focused on gestation. because it was believed that gestational mammary development had the greatest impact on subsequent lactation performance. Only two studies have examined pre—pubertal nutrition on mammary development (Crenshaw. 1990; Sorensen. 1993). The effect of 35 alternating restricted and ad libitum high—energy diets during the grow—finish and gestation phases on milk production was examined by Crenshaw in 1990. The restricted treatment used 30% sunflower hulls as a nutrient dilutent to dilute energy to 70% of that fed to control gilts. while the compensatory diet contained sunflower oil to achieve elevated energy at 115% of that fed to control gilts. Diets were alternated during two 3-wk periods and two 5 wk periods. At 21 days of lactation. parity one sows receiving alternating diets during rearing and gestation produced approximately 36% more milk as measured by weigh-suckle— weigh. and weaned heavier pigs when compared to control females fed a conventional corn-SBM diet continuously. It is unknown if the results achieved by Crenshaw (1990) were primarily a result of restricted feeding during the pre- pubertal phase. the gestational phase. or if restricting energy intake during both phases played an equal role in the results. It is also possible that the high-energy diet containing sunflower oil contributed to the mammary growth. A second study by Crenshaw (1990) examined the effects of a phase feeding regimen during the grow—finish phase and gestation phase on first lactation sow performance. by limit feeding gilts. In the first experiment sunflower hulls were used as an energy dilutent to restrict nutrient requirements. In the second experiment. daily feed intake was reduced during the restricted phases of the phase feeding regimen. During the grow—finish phase. gilts were 36 fed 5% of their body weight. as determined by weighing control gilts weekly. During gestation. gilts were fed 1.4 kg/d day during the restricted phase. and 1.8 kg/d during the compensatory phase. Diets were formulated to provide 75% and 115%. respectively. of the lysine and metabolizable energy intake of the conventional diet. Control gilts were allowed ad—libitum intake during the grow-finish phase. and 1.8 kg/d of the conventional diet during gestation. Phase feeding gilts through limiting intake had no effect on milk yield or litter weight gains. In a similar fashion to Crenshaw‘s second study. Sorensen and coworkers (1993) limited feed intake and reared gilts using a control. 75% control. and semi ad libitum between 42 d of age and 180 d of age. The semi ad libitum rearing regimen allowed gilts ad libitum feed intake twice each day for 30 min intervals (Sorensen et al.. 1993). The semi ad lib group consumed the greatest amount of feed and gained the most weight by the end of the grow—finish phase. The 75% control consumed the least amount of feed and gained the least amount of weight. Milk yield estimates were collected from the first to fourth lactation and dietary regimen had no effect on milk production and litter weight at weaning. These studies imply that the method in which gilt energy intake is restricted may influence how the gilt responds to a restrictive feeding regimen prior to puberty. 37 Gastatjon In 1988. Weldon examined the effects of elevated energy and crude protein during late gestation (the second allometric growth phase) on mammary development in swine. At 75 d of gestation. gilts were assigned to receive either adequate or elevated energy. along with adequate or elevated protein. Total parenchymal DNA was 29.8% greater in gilts fed adequate energy as compared to gilts fed elevated energy. In this study. protein levels did not appear to affect mammary development (Weldon. 1988). Head and Williams (1991) showed that high energy-low protein diets during gestation impaired mammary development. and were a result of excess energy. and not protein. Similar results involving elevated protein were also seen by Kusina and coworkers (1998a). In this study. gilts fed excess protein to achieve lysine intakes of 16g/d from 25 d to 105 d of gestation showed no increase in mammary development as measured by parenchymal DNA and RNA on d 110 of gestation. However. elevated protein during gestation led to increased milk production and increased litter gains (Kusina et al.. 1998b). Because there was no improvement in mammary development as indicated by DNA and RNA. it was hypothesized that the increased milk production may have been a result of adequate protein stores during gestation. to maximize milk yield during lactation (Kusina et al.. 1998b). It is also important to note that increased protein intake during gestation and during lactation also increased 38 feed intake during lactation. Although increased protein was fed during both gestation and lactation. there was no interaction between phases on the results. Increasing protein during both gestation and lactation may play a role in optimizing milk production. and may be a result of increased lactational feed intake. Contrary to the results of Weldon (1988). Howard (1995) found that excess energy had no effect on total mammary parenchymal DNA. The conflicting results between the two experiments were hypothesized to be a result of the way which parenchymal tissue. DNA. and RNA were expressed. Weldon's results were expressed on a per teat and per kg maternal body weight basis. Maternal body weight of gilts used in Weldon’s trial was affected by dietary treatments. thus weight may have been a confounding factor leading to the differences noted between energy levels. However. when results of Weldon (1988) are expressed on a total basis. total parenchymal tissue. DNA. and RNA are similar for gilts fed excess and adequate energy. thereby indicating excess energy had no negative effect on overall mammary development. Conclusion Fiber is commonly used in gestating sow diets to prevent constipation. however the inclusion of fiber in grow—finish and lactation is avoided due to fiber decreasing 39 available energy. protein. vitamins. and minerals. Research in heifers and rats has shown a benefit of restricting rearing energy intake prior to puberty in order to promote mammary development and increase subsequent milk yields (Tucker. 1987). Fiber may be useful in rearing diets of replacement gilts in order to enhance sow lactational performance. Work by Crenshaw (1990) suggests that feeding gilts high fiber diets during the pre—pubertal phase leads to an increase in subsequent milk production. Further research is needed in this area to determine if a moderate feeding scheme during the grow—finish stage of production can impact first parity lactational performance. 40 LITERATURE CITED Allee. G.L. 1976. Dehydrated alfalfa to control intake of self—fed sows during gestation. Report of Progress No. 283. Kansas State Univ.. Manhattan. Anderson. R.R.. R.J. Collier. A.J. Guidry. C.W. Heald. R. Jenness. B.L. Larson. and H.A. Tucker. 1985. Lactation. Iowa State University Press. Ames. IA. Anugwa. F.O.I.. V.H. Varel. J.S. Dickinson. W.G. Pond. and L.P. Krook. 1989. Effects of dietary fiber and protein concentration on growth. feed efficiency. visceral organ weights and large intestine microbial populations of swine. J. 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King. 1981. Wheat shorts in diets of gestating swine. J. Anim. Sci. 52:551. 51 Chapter 2 ABSTRACT THE EFFECTS OF A HIGH-FIBER PRE-PUBERTAL FEEDING REGIMEN ON IGF—1 CONCENTRATIONS. MAMMARY DEVELOPMENT. LACTATION POTENTIAL. AND REPRODUCTIVE PERFORMANCE IN SWINE Two hundred fifty—four crossbred gilts were allotted to one of two rearing nutrition regimens (Moderate or Control) from 9 to 25 wk of age to determine the effects of a high- fiber diet fed intermittently on gilt growth and parity-one performance. The Moderate regimen utilized high and low— fiber diets to alternate phases of moderate and maximum growth during four periods. During periods one and three the high—fiber diet containing 35% ground sunflower hulls was fed for 3 and 5 wk. respectively. to slow growth. During periods two and four the low-fiber corn—soybean meal (CSBM) based diet was fed for 3 and 5 wk. respectively. to maximize growth. Control gilts were given ad—libitum access to CSBM—based diets during all of the four periods. After 25 wk of age. both treatment groups were managed similarly. Average daily gain was lower (P<0.01) for the Moderate gilts during periods one and three. and greater (P=0.03) for the Moderate gilts during period four. Moderate gilts had greater feed intake during period four (P<0.01). During periods one and three. feed efficiency was lower for Moderate gilts (P<0.01). Plasma concentrations of IGF-1 were decreased for Moderate gilts during period one and the first week of period three (P<0.01 and P=0.03. 52 respectively). However. there were no differences in plasma IGF-1 concentrations of Moderate and Control gilts during the last week of period three. At puberty. Moderate gilts weighed less than Control gilts (P=0.001: 136.5 kg i 1.56 versus 144.1 kg 1 1.74). Regimen had no effect on pubertal age. number born alive. birth weight. pre—weaning survival rate. and wean—to-estrus interval. Litter weight gain increased (P=0.02) between d 7 and 14 of lactation for Moderate sows as compared to Control sows. Feed intake during lactation for Moderate females was greater than Control females (P=0.02; 101.9 kg 1 2.84 versus 94.5 kg 1 3.20). Mammary tissue samples from Moderate gilts collected on d 110 of gestation had less (P=0.03) parenchymal tissue. and tended to have less (P=0.09) DNA than Control gilts. Altering gilt growth before puberty increased sow lactation feed intake and litter gains between d 7 and 14 of lactation. despite not improving pre-lactation mammary development. Keywords: Gilt. Sunflower hulls. Fiber.IGF—1. Mammary development. 53 Introduction Sow milk production is important for the health and survival of the litter. Increasing sow milk production can improve litter growth. and increases in litter weaning weights can decrease days to market. Research has focused on improving sow milk production by altering hormone concentrations and nutrition during lactation (Farmer et al.. 1992: King et al.. 1993: Toner et al.. 1996) and gestation (Weldon. 1988: Howard. 1995). In heifers. milk production during first lactation improves when pre-pubertal energy intake is limited (Park et al.. 1987). To date. two studies have examined the role of pre-pubertal nutrition on subsequent milk production in swine. Crenshaw (1990) saw a 36% increase in parity-one milk production when energy intake was restricted intermittently prior to puberty and during gestation. Contrary to these results. Sorensen and coworkers (1993) saw no increase in milk production over four lactations when feed intake was restricted to 75% of ad—libitum during rearing. In gilts. energy can be restricted in one of two ways: 1) limiting feed intake (Sorensen. 1993). or 2) inclusion of fiber in the diet (Crenshaw. 1990). The addition of fiber in the diet dilutes nutrient intake and provides gut fill for satiety. while it has been suggested that limiting feed intake can alter behavior because pigs do not achieve satiety (Hutson. 1989). Crenshaw (1990) intermittently fed 54 a diet containing 30% or 32.5% sunflower hulls during the pre-pubertal period and during gestation. and saw an increase in parity—one milk production. It is unknown whether the increased milk production was a result of the pre—pubertal or the gestational feeding regimen. or both. The objectives of this study were to determine the effects of a high fiber diet fed intermittently during the pre-pubertal. grow—finish period on circulating IGF—1 concentrations. mammary development. and parity-one lactation performance. Materials and Methods All procedures for this study were approved by the Michigan State University All University Committee for Animal Use and Care. The experiment was conducted at the Michigan State University Swine Farm from January 1998 through November 1999. Ekperimantaj zbsjgn ana’YTaatmants Two nutritional regimens from 9 to 25 wk of age. and four litter sizes in parity-one lactation were used in a 2 x 4 factorial arrangement. The two nutritional regimens were designed to evaluate the relationships among pre-pubertal growth pattern. pre—pubertal circulating IGF—1. and mammary gland development prior to farrowing when fiber is added to the diet. Litter size was standardized within 3 d post farrowing to 9. 10. 11. or 12 piglets. 55 Animals At a mean wt of 23.8 kg (63 d 1 7 d). gilts were scanned for backfat depth (BF) and loin-eye area (LEA) at the 10th rib (Ultrasound Scanner 200 Vet with ASP—18 linear probe. Pie Medical Equipment B.V . Maastricht. the Netherlands). Based on litter and weight. gilts were alloted to one of the two nutritional regimens: 1) Control. ad-libitum access to corn—soybean meal (CSBM) based diets: or 2) Moderate. alternating ad-libitum access to CSBM based diets containing 35% ground sunflower hulls. and the same CSBM diets fed to Control gilts. Diets were fed during four distinct periods. Periods one and two each lasted 3 wk. and periods three and four each lasted 5 wk (Table 1). During periods one and three. Moderate gilts were fed the 35% ground sunflower hulls diet. During periods two and four. Moderate gilts received the same CSBM diets fed to Control gilts during periods two and four (Figure 1). Control diets were formulated to meet or exceed National Research Council (NRC) 1988 recommendations for energy and amino acids. Moderate diets were formulated to contain 70% of the metabolizable energy. and 85% of the crude protein in the Control diets. Vitamin and mineral concentrations in all diets met or exceeded NRC (1988) recommendations. and were adjusted based on the expected feed intake (Table 2). During lactation. sows were provided one of four diets based on litter size (Table 3). Diets were formulated using 1998 NRC recommendations. and lysine concentrations were 56 adjusted to meet the requirements of the sow based on the size of the litter she was nursing. management Within 7 d of each dietary change for the four periods (at 3. 3. 5. and 5 wk. respectively) gilts in the grow- finish rooms were weighed and total feed disappearance by pen recorded to determine individual ADG and ADFI by pen. respectively. At the end of the four feeding periods. both Control and Moderate gilts were maintained on the last Control diet for an average of 17 d until being moved to the breeding area. At approximately 187 d of age gilts were moved from the grow-finish rooms to the breeding room. At this time. gilts were vaccinated against porcine parvovirus. erysipelothrix rhusiopathial. and leptospira bratislava using five cc of Farrowsure Bm (Pfizer Animal Health. Exton. PA). Moderate and Control gilts were mixed and no greater than 9 gilts were maintained per group pen (2.5 m x 3 m). Gilts were allowed ad-libitum access to a breeding CSBM diet (Table 4) and monitored daily at 0730 and 1630 for signs of estrus using the presence of a boar. At first estrus. gilts were weighed. scanned (1 7 d) for BF and LEA measurements. individually penned. and fed 2.3 kg of the breeding diet per day. Fourteen days prior to expected second estrus. feed offered was increased to 3.2 kg per d. Gilts not showing 57 first estrus by 285 d of age were removed from the experiment. Gilts were bred at second estrus with pooled Duroc semen using artificial insemination (AI). Gilts exhibiting standing heat in the morning were bred immediately. Gilts exhibiting standing heat in the evening were bred the following morning. Gilts were serviced each morning until no longer in standing heat. Bred gilts were weighed and moved to individual crates in the gestation room within 7 d of their last insemination. In gestation. all gilts were fed a diet containing 10% wheat bran (Table 4). During the first week of gestation. gilts were given 1.4 kg of diet per day. From wk 2 to 7. 8 to 13. 13 to 14. and 15 to farrowing. gilts were provided daily feed allowances of 1.8 kg. 2.3 kg. 2.7 kg. and 1.8 kg. respectively. Gilts in the gestation room were confirmed pregnant by monitoring for estrus 21—d post-breeding. Gilts returning to estrus a second. or third time were re-bred. Gilts returning to estrus a fourth time were excluded from the study. Pregnancy was confirmed 6 to 8 wk post-breeding using ultrasound (Renco Preg—ToneGL Renco Corp.. Minneapolis. MN). Gilts that aborted during the gestation period were retained for one—additional opportunity for a successful pregnancy. Gilts that had been bred. were not pregnant. and failed to shows signs of return-to—estrus were culled for failure to farrow. Five cc of Prosystem® 4*3 (Intervet Inc.. Millsboro. DE). a clostridium/E—coli. vaccine. was administered in the Trapezius muscle at 5 and 2 wk prior to farrowing. One week prior to expected farrowing date (d 114). gilts were scanned for BF and LEA and moved to individual farrowing stalls equipped with a heating pad. and a heat lamp. Sows were offered 1.8 kg of the lactation diet (dependent on litter size) the first feeding after farrowing. Feed offered was increased in 0.5-kg increments at morning and evening until ad—libitum intake was reached. Total feed offered was recorded for each sow. Diets were adjusted if litter size changed due to piglet death. Sows rearing eight piglets. because of piglet mortality. were maintained on the same diet formulated for sows rearing nine piglets. Data from these sows and litter was collected and retained for analysis. Sows were weighed after farrowing and individual pig weights were recorded at 0. 7. 14. and weaning. Litter weights were obtained post—cross-fostering on 101 of the 133 total litters. Within 3 d post farrowing. litters were processed (iron injections. vaccinations. castration. ear notching. etc.). and size adjusted to 9. 10. 11. or 12 piglets by cross-fostering. Litters were weaned between 17 and 24 d. to achieve an average weaning age of 21 d. Sows were weighed and scanned for LEA and BF measurements at weaning. After weaning. return—to-estrus data was collected for each sow. 59 Feed Analysis All diets were sampled periodically. pooled. and a sub— sample was collected from each diet. Sub-sample were finely ground using the Cyclotron Sample Mill (Foss Tecator. Haganos. Sweden) and analyzed for gross energy (GE) (model 1241 adiabatic calorimeter. Parr Instruments. Moline. IL). nitrogen (N) (model FP-2000 carbon/nitrogen analyzer. LECO. St. Joseph. MI). and ether extract (AOAC. 1984). Crude fiber (CF) was determined by the ANKOM procedure (Komarek et al.. 1996). Feed samples were digested in nitric and perchloric acid for calcium (Ca) and phosphorous (P) determination (Hill et al.. 1983). Phosphorus was determined by the method of Gomori (1942) with concentrations measured spectrophotometrically at 700nm (Beckman DU-7000. Schaumburg. IL). Calcium concentrations were determined by method of Hill and coworkers (1983) with lanthium chloride substituted for strontium chloride. and using atomic absorption spectrometry (UNICAM SOLAAR32 Spectrometer. England). Instruments were standardized by appropriate external standards from the National Institute of Standards and Technology. Lysine was analyzed according the Pico-Tag® method for amino acid analysis (Hagen et al.. 1992). Analysis of samples was performed in duplicate. Blood Collection and Analysis Sixteen gilts (8 Control. 8 Moderate) were randomly selected for collection of blood samples 1 wk prior and 1 wk 60 post dietary change for each of the four experimental ‘dietary periods. The same 16 gilts were bled at each collection period. Samples were collected in 10-mL sodium heparinized Vacutainers® using 4 cm. 20 gauge needles (vacutainers and needles. Becton Dickinson and Co.. Franklin Lakes. NJ). Gilts were not fasted prior to sampling. Samples were immediately placed on ice. centrifuged at 1500 x g for 15 min. plasma removed and frozen at —80°C. until analysis for IGF-1 concentrations. Plasma samples were removed from the freezer and allowed to thaw at room temperature for 1 hr. An IGF-1 radioisotopic assay (RIA) 100T kit (Catalog No. 40-2100. Nichols Institute Diagnostics. San Juan Capistrano. CA) for human plasma was used for quantitative determination of IGF- 1 concentration in plasma. This kit had been previously validated for use in swine (White et al.. 1991). Plasma samples were precipitated with acid-ethanol to separate soluble IGF-1 from IGF binding proteins. The acid-ethanol extraction method was altered to achieve a sample dilution of 1:113 with the reagent buffer (60 ul of sample:240 ul of acid—ethanol. all remaining steps of the acid-ethanol procedure were performed in full volume as outlined in the RIA kit). The RIA procedure was then carried out at half of the manufacture’s suggested volume. Samples were assayed in duplicate and samples were counted for 5 min using the 190 Gamma Tracm (Tm Analytical. Tampa. FL). Percent binding for sample counts was determined. values were log transformed 61 and plotted along the ordinate of a standard curve graph using DNA-recombinant IGF-1 standards. The corresponding abscissa value was read and multiplied by the dilution factor (113) for acid-ethanol extraction to determine the IGF-1 concentration in ng/mL. Duplicate samples with a CV greater than 15% were repeated. Inter-assay variation was 11.4%. and intra—assay variation averaged 6.7%. mammany'lissue Collection and’Analysis Twelve gilts (6 Control. 6 Moderate) were slaughtered on d 108 to 112 of gestation to obtain mammary tissue. Selected gilts were between 330 and 370 d of age. and possessed 14 teats (seven per side). Gilts were slaughtered following MSU standard slaughtering procedures. Following slaughter. the entire mammary gland was removed. Fetus number was recorded. Mammary glands from gilts with less than five fetuses were discarded. Mammary glands were weighed and separated into right and left halves. The left half was discarded. The right half was weighed and frozen by immersing in a mixture of dry ice and acetone. Glands were then stored at —20°C until analysis. Frozen mammary glands were cut into 1.5-cm slices using a band saw. Teats. skin and lymph nodes were removed using a scalpel. and glands were separated into parenchymal and extraparenchymal tissue while frozen. The parenchymal and extraparenchymal tissue was distinguished by color. Extraparenchymal tissue was white. and the parenchymal 62 tissue was pink. After separation. tissue was placed on dry ice until the entire gland had been dissected. Individual tissue components were weighed. and the parenchymal tissue was stored at —20°C until homogenization. Frozen parenchymal tissue was placed in a plastic bag and broken into smaller pieces using a metal hammer. placed in a Waringm commercial blender (Model CB-5. Waring Products Co.. Winsted. CN). and submerged in liquid nitrogen. The tissue was homogenized at high speed for 30 sec. The resulting powder was sifted through a 1—mm screen. kept on dry ice. and tissue remaining in the screen was re- homogenized until only 10% of the original tissue was retained. Powder samples were mixed. and a representative sample from each gland was obtained and stored at —20°C until analysis. RNA and DNA were determined by the method of Tucker (1964). Duplicate 100—mg samples of frozen. powdered tissue were weighed into 13.5 ml. high speed Nalgenem centrifuge tubes (Nalge. Rochester. NY). To remove the lipid component. samples were extracted with 10 mL 95% ethanol under constant agitation (225 shakes/min) for 24 h. Samples were centrifuged (1500 x g. 15 min). and the supernatant was discarded. The ethanol extraction was repeated. Ether (10 mL) was added to the sample. samples were vortexed. centrifuged (35.000 x g. 20 min). and the supernatant discarded. Tubes were placed in the hood for 1 hr to allow excess ether to evaporate from the pellet. 63 Methanol chloroform (2 1) mixture was added. the samples were placed under constant agitation (225 shakes/min) for 24 h. centrifuged (1500 x g. 30 min). and the supernatant aspirated. The samples were placed under constant agitation (225 shakes/min) an additional 24 hr with 10—mL anhydrous ether. Samples were centrifuged (35.000 x g. 20 min). supernatant aspirated. and placed in the hood to allow excess ether to evaporate. Samples were placed on ice. and extracted twice with 5 mL 10% tri—chloracetic acid (TCA) to remove low molecular weight. acid soluble components. After TCA was added. samples were vortexed. centrifuged (35.000 x g. 20 min). and supernatant discarded. The remaining precipitate was washed with 5 mL 95% ice-cold ethanol saturated with sodium acetate (0.07 g sodium acetate was added per 1 mL of ethanol. brought to 100°C. and mixed for 30 min). to remove any remaining TCA. Samples were then digested with 2 mL 1 N potassium hydroxide (KOH) for 15 h at 37°C to hydrolyze the ester bonds of RNA to yield nucleotides. and separate RNA from DNA. Samples were cooled in ice water. acidified with 0.3 mL 6 N hydrochloric acid (HCl). and 5 mL 10% perchloric acid (PCA). Acidification with HCL allowed precipitation of DNA. while the nucleotides from RNA hydrolysis remained in solution. Samples were centrifuged (35.000 x g. 20 min). and the supernatant was aspirated and saved. The precipitate was re-washed twice with 5% PCA. and the three supernatant portions combined for RNA analysis. The 64 remaining precipitate was extracted with 5% PCA at 70°C for 15 min to split phospho—diester bonds and breakdown hydrogen bonds holding together the two strands of DNA. Samples were centrifuged (35.000 x g. 20 min). and the supernatant was aspirated and saved. The precipitate was re—washed twice with 5% PCA. and the three supernatant portions combined for DNA analysis. Purified yeast RNA and highly polymerized calf thymus DNA (Sigma®. St. Louis. M0) were used as standards for RNA and DNA. respectively. The DNA standard (0.01 g) was dissolved in 100 mL 5% PCA. and concentrations of 5. 10. 20. 30. 40. 50. and 60 ug DNA/mL of deionized water at a final volume of 5 mL was used to plot the standard curve. The RNA standard (0 01 g) was dissolved in 100-mL 5% PCA and heated in a 37°C water bath for 15 min. Concentrations of 4. 8. 16. 24. 32. 40. 48. 56. and 64 ug RNA/mL of deionized water were made to a final volume of 10 mL. These concentrations of RNA/mL were two times the final concentrations because the standard RNA curve solutions were diluted 1:1 with the orcinol procedure. For the orcinol procedure. 3 mL of the RNA sample extracts and standard curve solutions were diluted with 3 mL of orcinol reagent. The orcinol reagent was made by dissolving 1.20 g of orcinol (Sigama®. St. Louis. M0) to a volume of 120 mL with ferric chloride solution (1.6 g ferric chloride dissolved with 1 L HCL). The orcinol reagent was heated in a 70°C water bath for 10 min. After the orcinol reagent (3 mL) was added to 3 mL of 65 the RNA sample extracts and standard curve solutions. solutions were incubated in a 100°C water bath for 30 min. DNA and RNA was analyzed using a microplate spectrophotometer (SPECl‘RAmax19°® Mi crop late Spectrophotometer. Molecular Devices Corp.. Sunnyvale. CA). Absorbency was measured at 670 nm and 268 nm for RNA and DNA. respectively. Results for RNA and DNA were corrected for the dilution factor and expressed per gram of parenchymal mammary tissue. SYatistical Analysis Grewtn.Perfbnmance. Data were analyzed using the analysis of variance procedures of SAS (Proc Mixed: 1997). Group and diet were fixed effects. and pen was considered a random effect. Degrees of freedom were determined using the method of Satterthwaite (1946). Analysis of variance was used to test regimen (Control and Moderate). period (1.2.3.and 4). and regimen*period interactions on the independent performance variables (ADG. ADFI. feed efficiency. age at pubertal estrus. weight at estrus. BF at estrus. LEA at estrus. and IGF-1 plasma concentrations taken pre and post dietary changes). The main difference between treatments. and regimen*period interactions were detected by comparison of least square means. Culling data was analyzed using the Proc Freq procedure of SAS (1997). Chi-square was used to test regimen (Control and Moderate) on stage of 66 culling. and reasons for culling. Difference between means was considered significant at P<0.05. mammaryhflevelqpmentz jData were analyzed using the general linear model analysis of variance procedure of SAS (Proc GLM: 1997). Estrus at time of breeding had no statistical significance (P=0.50) on measures of mammary development and was removed from the statistical model. Analysis of variance was used to test the dietary regimen (Control and Moderate) effect on total gland weight. right side gland weight. parenchymal and extraparenchymal tissue weight. DNA. RNA and RNA/DNA ratio. Linear and quadratic regression covariates for fetus number were included in the statistical model for analysis of mammary tissue. The main difference between treatments was determined by comparison of least square means. Difference between means was considered significant at P<0.05. .Repredactive anaflzactatienal.Perfenmance. iData were analyzed using the general linear model analysis of variance procedures of SAS (Proc GLM; 1997). Estrus bred had no effect on any reproductive or lactational performance measures and was not included in the statistical models. Analysis of variance was used to test the dietary regimen (Control and Moderate) effect on gilt breeding age. breeding weight. farrowing age. farrowing weight. farrowing BF. and farrowing LEA. Interactions between regimen*litter size 67 were tested on the independent variables of litter weights (d 0. 7. 14. 21. and weaning). litter gain. sow feed intake. sow weight. LEA and BF at weaning. and sow’s return-to- estrus. Lactation length and average litter weight post cross-fostering or at birth if no cross-fostering occurred were used as a non-classified covariates in statistical models analyzing subsequent litter weights and litter gains. Differences between regimen and adjusted litter sizes were detected by comparison of least square means using the studentized t-test for probability. Interactions between rearing regimen and adjusted litter size at lactation were not significant. therefore. only main effects of rearing regimen were reported. Difference between means was considered significant at P<0.05. Results calling Of the 257 gilts allotted to the feeding trial at 9 wk of age. 121 gilts were culled from the experiment. Three gilts were culled during the grow-finish phase. 20 gilts from grow-finish to breeding. and 58 gilts from gestation through parity-two breeding (Table 5: Figure 2). Thirty-one gilts farrowed. but were excluded from the study because of low number born alive. and no piglets were available for cross-fostering. Parity-one performance data was collected from 133 females. Comparing Moderate and Control females. a total of 28 Moderate gilts and 53 Control gilts were culled 68 from the time rearing regimens were initially imposed until sows were bred for their second parity (P<0 01). Culling from selection at end of the 16 wk trial to breeding (P<0.05). and culling from gestation to parity—two breeding (P<0.01). were also greater in Control females. The three most common reasons for culling gilts were: 1) failure to conceive their first litter by third service (11 Moderates. 12 Controls). 2) unsound feet and leg structure (2 Moderates. 10 Controls). and 3) failure to farrow (gilts that were bred. but did not show signs of return-to—estrus; 4 Moderates. 7 Controls) (Figure 3). Control females had a greater incidence of culling for locomotive failure (unsound feet and legs. and broken legs) as compared to Moderate females (13 versus 2. respectively: P<0.01). Growtn.Perfermance Initial weight of gilts was not different between Control and Moderate groups. After one period of feeding the high-fiber diet. Control gilts weighed greater (P<0.05) than Moderate gilts. and continued to weigh greater than Moderate gilts through the 16 wk feeding trial (Figure 4). There were no differences in ADG for the overall duration of the 16—wk grow-finish portion of this experiment. However. overall ADFI was greater and overall feed efficiency was less F/G for Moderate gilts (P=0.04 and P<0 01. respectively) (Table 6). Differences between Control and Moderate groups were identified within individual periods 69 (Table 6). Average daily gain was less (P<0.01) for Moderate gilts than Controls in periods one and three when the sunflower diet was fed. but greater (P=0.03) in period four. Average daily feed intake tended (P=0.06) to be lower for Moderate gilts during period one. but tended to be higher for Moderate gilts during period two (P=0.09) and was higher in period four (P<0.04). Feed efficiency was different between nutritional regimens during periods one. three. and four. With Moderate gilts being less efficient during periods one and three (P<0.01). and more efficient during period four (P<0.01: Table 6). £Yasma [GEL] Moderate gilts had lower mean plasma IGF—1 concentrations during period one and after being switched to the fibrous diet in period three (P<0.01. and P=0.03. respectively). This decrease corresponded to decreased energy intake due to the addition of sunflower hulls to the diet. When Moderate gilts were switched from the high—fiber to the CSBM based diet (transition from period one to two). plasma IGF-1 concentrations increased (58 ng/mL to 184 ng/mL). However. plasma IGF-1 concentrations did not increase the second time gilts were switched from a high- fiber to CSBM diet (period three to four). Plasma IGF-1 concentrations of Moderate gilts were not affected by dietary regimen during the last week of period three. and were greater than plasma IGF—1 concentrations of Control 70 gilts (P=0.04: 192 ng/mL versus 130 ng/mL. SE 15.31). During the last week of period three. and during period four. Control plasma IGF-1 concentrations decreased. while Moderate plasma IGF—1 concentrations increased (Figure 5). .ReprodUctive.Develqpment Mean age at which gilts were moved from the grow—finish rooms to the breeding room did not differ (Table 7). Days required for gilts to reach puberty after being moved did not differ between groups. Backfat depth. LEA and age at puberty were not different for Moderate and Control gilts: however. Moderate gilts weighed less at puberty (P<0.01) (Table 7). hammanyubevelqpment Data of two gilts. one of each treatment. was not included in the analysis because they each had less than five fetuses. A trend existed for Control mammary glands to be greater in total gland weight (P=0.10). right side gland weight (P=0.09). and total DNA (P=0.09) when compared to mammary glands from Moderate gilts. Parenchymal tissue weight of Control gilts was greater (P=0.03) than that of Moderate gilts. Other indicators of mammary development. including DNA and RNA concentration (mg/g of parenchymal tissue). extraparenchymal tissue weight. total RNA. RNA/DNA ratio. and DNA and RNA corrected per kg of maternal body 71 weight and per teat number. did not differ between treatments (Table 8). Lacta tienal Performance Total feed intake in lactation. corrected for lactation length and litter size weaned. was different between Moderate and Control sows. with Moderate sows consuming more total feed during lactation (P=0.02). All measures of sow body condition (absolute and change) during lactation were similar for Moderate and Control nutritional rearing groups (Table 9). There was also no difference between these two groups in their return—to—estrus response post-weaning. Number born alive. number of stillborn piglets. number of mummies. and pre-weaning survival percentage were not different for Moderate and Control groups (Table 10). Litter weight on d 0 and 7 did not differ between Moderate and Control groups. At d 14. litters from Moderate sows were 2.4 kg heavier than litters from Control sows (P=0.02). and this difference was also seen as a trend at weaning (P=0.07) (Table 11). Litter gains from d 0 to 7. and from d 14 to weaning were not different between Moderate and Control groups: however. litter gain from d 7 to 14 was greater for the Moderate treatment group (P=0.02) (Table 12). Discussion The hypothesis of this experiment was that intermittently feeding a high-fiber diet to promote periods of moderate and maximum growth during the grow-finish phase would alter the IGF—1 profile of the growing gilt. and lead to an improvement in mammary development and subsequent parity-one lactation performance. Growth ana’fleprednctive.Perfenmance Moderate diets fed during periods one and three. were formulated to contain 70% of ME of Control diets. Previous research has shown that when MB is restricted by 30%. and CP is fed at 120%. only 85% of the protein is utilized for protein accretion. the rest undergoes deamination (ARC. 1980). Therefore. CP was restricted to 85% of that estimated to be supplied by the CSBM based Control diets during periods one and three (Table 2). Diets were formulated based on research showing that pigs fed a high— fiber diet increase feed intake to compensate for the decreased energy intake (Kennely and Aherne. 1980). However. in the current experiment gilts did not increase feed intake when the high—fiber diet was fed. Based on ADFI. it is estimated Moderate gilts consumed 65% of ME. and 75% of CP during period one as compared to Control gilts. During period three. the estimated ME and CP intakes of Moderate gilts were 65%. and 85% of that consumed by Control 73 gilts. respectively. During periods two and four. Moderate gilts intake was estimated at 105% and 114. respectively. of Control gilts estimated intake. The inclusion of sunflower hulls in period one and three diets depressed ADG. as shown in previous research involving various fiber sources (Kass et al.. 1980: Hale and Utely. 1985). In the current experiment. ADFI was decreased by dietary fiber during period one. but was not different from the Control group during period three (Table 6). This suggests that when duration of feeding fiber exceeds 3 wk. feed intake is not impaired. Similar results have been observed previously by Hale and Utely (1985). Compared to feeding a low-fiber CSBM diet. continuous feeding of fiber throughout rearing had no effect on ADFI. while feeding fiber for only two weeks decreased ADFI. Research has shown that stomach weights increased after only 17 d of feeding a high—fiber diet. and regression back to previous weights did not occur until after d 32 of being switched to a low—fiber CSBM diet once again (Anugwa et al.. 1989). Therefore. when pigs were switched to the high- fiber diet in period three. a residual effect from earlier feeding of the high~fiber diet during period one may have occurred. Stomach weight may not have fully regressed by the start of period three. and thus the stomach may have already been partially adapted to digestion of the high— fiber diet resulting in ADFI in period three of Moderate gilts being similar to those of Control gilts. 74 When the CSBM diets of the Control regimen were fed to the Moderate group ADFI tended to be greater than Controls in period two (P=0.09) and was greater than Controls in period four (P<0.01). It appears that pigs may have compensated for the decrease in nutrient intake during periods one and three by consuming more feed during periods two and four. Accompanying the increase in ADFI during period four with the Moderate regimen. was a greater ADG than Controls. There was no indication of a compensatory phase of gain occurring during period two for Moderate gilts. Reports of compensatory growth following periods of growth restriction are conflicting. Earlier research involving dietary restriction for 21 d. showed no compensatory gain after gilts were switched from a high— fiber (80% alfalfa meal) to a low—fiber. corn—SBM diet (Pond and Mersmann. 1989). Conversely. Fischer and coworkers (2000) saw an increase in the gain of gilts given ad libitum access to feed after gilts were being restrictively fed only maintenance amounts of nutrients. above that of gilts provided ad libitum access to feed continuously. Feed efficiency was also greater. In the current study. feed efficiency was impaired during feeding of the fiber diet. This is in agreement with the majority of fiber studies (Kass et al.. 1980: Kennelly and Aherne. 1980: Pond and Mersmann. 1989: Pond et al.. 1989) which show that feed efficiency is poorer when high— fiber diets are fed. When gilts were switched to the low- 75 fiber CSBM diets during periods two and four. feed efficiency did not differ between Control and Moderate gilts. Although ADFI and ADG was greater for Moderate gilts than Control gilts during period four. Moderate gilts were not more efficient in converting feed to gain during what appeared to be a time of compensatory growth. In the current experiment. Moderate gilts were not as heavy as Control gilts at puberty (136.6 kg 1 1.56 versus 144.1 kg 1 1.74). A delay in first estrus is often related to a decrease in body weight associated with restricting feed or energy intake (Friend. 1976: den Hartog and Noordewier. 1984): however. there were no differences in age at first estrus associated with the feeding regimen employed in the present study. Crenshaw (1990) also reported that intermittent feeding of a high-fiber diet during rearing had no effect on pubertal age. Intermittent restriction of energy intake. as compared to prolonged restriction of energy intake during rearing. does not delay age at puberty. In swine production. increased age at first estrus is undesirable. leading to increases in non—productive days and costs of production. At breeding. weight was not different between groups (Table 8). Because both groups of gilts were individually fed the same amount of feed from first estrus to breeding. and time from first estrus to breeding was similar. it appears Moderate gilts were more efficient in converting feed to gain during the time from puberty to breeding. 76 calling'lncidence Culling incidence was recorded for Moderate and Control gilts from the beginning of the grow—finish period until after first lactation (Table 5: Figure 2). In the present study. unsound feet and legs and failure to conceive were the two most common reasons for culling (Figure 3). There was an increase incidence of culling during rearing and pre- breeding for the Control gilts versus Moderate gilts due to locomotive failure. Our results agree with previous research which indicated that gilts fed ad-libitum or increased energy during rearing. as compared to restricted energy intake. had a higher incidence of culling primarily during rearing as a result of leg weakness (den Hartog and Noordeweir. 1984; Danielsen et al.. 1993). Although the relationship between increased energy intake and increased culling due to lameness has been documented. it is not fully understood why this occurs. Maximizing growth of gilts during the rearing period is a common practice used to achieve early age at puberty. However. high energy intakes also results in an increase in mature body size at an earlier age. Although weights between Moderate and Control gilts were not different at breeding. Control gilts were heavier at each period during the grow-finish phase and at first estrus. Control gilts. therefore. reached a greater weight at an earlier age. The skeletal structure may be unable to support this increase in size at an early age. and therefore the greater stress to 77 the skeletal system may result in an increase in lameness in rapidily grown gilts. Number culled due to reproductive failure was similar between Control and Moderate gilts (Figure 3). This is in contrast to research which shows an increased incidence of gilts exhibiting behavioral anestrus and a lower pregnancy rate after first insemination when fed high energy during rearing (den Hartog. 1984). and a lower conception rate for parity-one gilts subjected to dietary restrictions during rearing (Kirchgessner et al.. 1984). PYasma 16%;] Blood concentrations of IGF—1 in recently weaned pigs are low compared with other species at similar stages of postnatal development (Owens et al.. 1991). Previous research has reported that IGF—1 concentrations in pigs rises to peak concentrations at approximately 13 wk of age. and then declines steadily as market age approaches (Holck et al.. 1998: Frank et al.. 1998). Insulin like growth factor-1 concentrations of Control gilts in the current study followed a similar age pattern (Figure 5). In swine. Rozeboom (1992) reported that bred gilts switched from a high energy to low energy diet had decreased IGF-1. switching from a low to high-energy diet increased IGF—1 concentrations. In this study. decreased energy intake likewise resulted in decreased IGF-1 during period one and the first week of period three. However. IGF-1 78 concentrations were increased for Moderate gilts during the last week of period three. which was the end of a low—energy intake period. It is unknown why IGF-1 concentrations began to increase toward the end of the last high—fiber period. when they had previously decreased when energy intake was lowered. Toward the end of period three. the pigs may have adapted to the diet and increased intake. and thus may not have been as restricted as what was seen in period one and the first week of period three. Adaptation to the diet. may have led to feed consumption. growth rate. and IGF—1 concentrations of Moderate gilts all being greater than Control gilts at the end of period three. Feed intake and growth were not determined on a weekly basis. rather on a period basis. and so there was no measure of feed intake by week. which would support this speculation. hammanyuflevelqpment Total gland weight and right side gland weight tended to be greater (P<0 10) for Control gilts. and parenchymal weight of Control gilts was greater (P<0.03) than the weight of the same tissues collected from Moderate gilts (Table 9). Because there is no clear distinguishing line in the separation of parenchymal and extraparenchymal tissue. and because the parenchyma branches into the fat pad (Tucker. 1987) the parenchymal weight still includes portions of the extraparenchymal tissue. Therefore. weight of individual 79 tissues is not as precise of an indicator of mammary secretory potential as DNA and RNA. Control gilts tended (P<0.09) to have more total DNA than Moderate gilts (Table 9). Inversely. Weldon (1988) saw impaired mammary development from gilts fed high energy during late gestation. when RNA and DNA were adjusted for teat number and maternal body weight. Howard (1995) saw no difference between total RNA and total DNA from gilts fed adequate or elevated energy during gestation. In the second experiment RNA and DNA was expressed on a total basis and not corrected for teat number and maternal body weight. When Weldon’s (1988) results were expressed on a total basis. RNA and DNA between dietary treatments was not different. In the current experiment. all gilts had the same number of developed teats. Results of this experiment suggest that the pre—pubertal feeding regimen which restricted energy intake. may have limited mammary development in gilts. Mammary development in cattle is increased with restrictive feeding regimens prior to puberty (Peri et al.. 1993). In the current study. the relationship between IGF—1 profile during rearing and subsequent mammary development could not be clearly determined. On two occasions. the end of period one and the first week of period three. IGF—1 concentrations of Control gilts exceeded those of Moderates. Conversely. on one occasion. the last week of period three. Moderate gilts had greater circulating IGF-1 concentrations 80 than Controls. As mentioned above. Control gilts tended to have more mammary DNA than Moderates. The role of IGF—1 in mammary development in cattle is likewise not well understood. Synthesis of DNA by bovine mammary tissue in— vitro is positively related to IGF-1 concentration (Oka et al.. 1991). However. restricting energy intake of heifers during rearing decreases circulating IGF—1. while enhancing mammary development (Capuco et al.. 1995). Litter.Perfenmance In the current experiment. litter weights were used as an indicator of milk production. Lewis and coworkers (1978) previously stated that litter weights were not the best indicator of milk production due to environmental and genetic factors. However. these factors. along with litter size were controlled. On d 14 of lactation. litters from Moderate gilts were heavier than litters from Control gilts (Table 11). Notably. Moderate litters gained more between d 7 and 14. as compared to Control litters (Table 12). It appears that between d 7 and 14. Moderate sows produced more milk than their Control counterparts. Litter gains between d 14 and weaning were not different between Moderate and Control groups (Table 12). and there was only a trend (P=0.07) for Moderate litters to weigh more at weaning than Control litters. Differences in weight gain did not increase between Control and Moderate groups as compared gains between d 7 to 14. Litter weights at weaning were 81 most variable of all weights recorded. Therefore. after d 14. milk production of Moderate sows appears not to differ from Controls. In the present study. mammary development at d 110 of gestation is not an indicator of subsequent milk production during parity—one lactation. It is unknown why the discrepancy between d 110 mammary development and parity—one milk production occurred. However. it may be a result of 1) rearing nutrition affecting parity—one mammary growth during lactation when milk production is in greatest demand to feed the litter. 2) rearing nutrition affecting parity—one appetite supplying more nutrients for milk production. or 3) rearing nutrition potentially altering mammary development during lactation. as feed intake is increased. The mammary gland of the pig continues to grow from d 0 to 21 of lactation (Kim et al.. 1999). Because litter weight gain was only greater during d 7 to 14. it appears that this is when Moderate females produced more milk. If rearing nutrition did affect parity-one mammary gland growth of Moderate sows occurring during lactation. litter gains would be expected to be maintained between d 14 and weaning when litter demand for milk is even greater. However. litter gains of Moderate sows as compared to Control sows were not different at this time. Therefore. it appears rearing nutrition did not stimulate mammary gland growth of Moderate sows as compared to Control sows during lactation. 82 The difference in milk production as measured by litter weights maybe a result of the difference in feed intake during lactation. Moderate sows consumed more feed during lactation. than Control sows. Crenshaw (1990) saw a 36% increase in milk production as measured by weigh-suckle— weigh for gilts reared under an intermittently fed high- fiber restricted regimen. and in that study gilts also consumed more feed during lactation. In the current experiment. the differences in feed intake may be a lingering result of the dietary restrictions imposed during the pre-pubertal period. When Moderate gilts were given ad— libitum access to the low—fiber CSBM diet during periods two and four. they consumed more feed than Controls. Gilts were allowed ad—libitum intake from the end of the experimental regimen until first estrus. after which they were individually fed equal amounts. Feed intake was also limited during the gestation period. It was not until lactation that gilts were again allowed ad—libitum access to feed. Because feed intake was controlled through the estrus. breeding. and gestation periods. moderate gilts may not have consumed enough feed during the ad-libitum periods to compensate for the periods in which intake was restricted earlier in life. Therefore. Moderate gilts may have been experiencing a compensatory response during lactation to account for earlier energy and growth restriction. If this is the case. it is uncertain whether the increased milk 83 production of Moderate gilts would be sustained through subsequent parities. Implications Intermittent inclusion of fiber in diets fed to gilts during rearing is beneficial in reducing culling due to locomotive problems and increasing milk production in parity-one lactation. An increase in milk production leads to heavier pigs on d 14 of lactation. and could be beneficial for early weaning programs. However. it is uncertain whether similar results would occur during subsequent lactations. Imploring a moderate feeding regimen which includes fiber. during rearing requires early identification of replacement gilts. separate rearing facilities. and an available fiber source. all of which can add to the cost of producing replacement females for the breeding herd. Table 1. Diets fed during the four pre-pubertal feeding periods (Compositions of diets A. B. C. D. and E are shown in Table 2) Nutritional Period Regimen 1 2 3 4 Duration 0 to 3 4 to 6 7 to 11 12 to 16 Control A A C E Moderate B A D E 85 Table 2. Composition of experimental grow-finish diets (as— fed basis) Diet Ingredient. % A B C D E Corn 62.26 36.20 71.95 39.57 75.87 Sunflower hulls — 35.00 - 35.00 - Soybean meal. 44% CP 30.26 22.42 20.56 19.26 17.96 Mono—Dical—Phos. 2.07 2.73 1.98 2.52 1.74 21% P Ground limestone 0.84 0.55 0.81 0.55 0.83 Choice white grease 3.00 1.50 3.00 1.50 2.00 MSU Vit premix“ 0.60 0.60 0.60 0.60 0.60 MSU TM premixb 0.50 0.50 0.50 0.50 0.50 Salt 0.50 0.50 0.50 0.50 0.50 L-lysine HCL. 78.8% — — 0.10 - - :1 . J E J . Gross energy.Kcal/kg 4014.80 4019.69 4271.16 4056.72 4101.54 Crude protein. % 19.11 14.40 15.64 14.42 14.88 Crude fiber. % 9.75 31.16 6.41 25.22 4.44 Ether extract. % 13.17 13.17 13.86 13.28 13.29 Lysine. % 0.99 0.69 0.75 0.66 0.70 Calcium. % 1.23 0.75 1.02 0.85 1.07 Phosphorous. % 0.78 0.47 0.66 0.84 0.70 Supplied per kilogram of diet: vitamin A. 5511.49 IU: vitamin D. 551.15 IU: vitamin E. 66.00 IU: vitamin K. 4.40 mg: riboflavin. 4.40 mg: pantothenic acid. 17.60 mg: niacin. 26.40 mg: vitamin Bu. 33.00 ug thiamine. 1.10 mg: vitamin By 990.00 ug. Supplied per kilogram of diet: Mn. 11.00 mg: Fe. 11.00 mg: Cu. 11.00 mg: I. 150 ug: Zn. 100 mg: Se. 300 ug. Table 3. Composition of lactation diets (as-fed basis) Dietsa Ingredient. % 9 10 11 12 Corn 69.74 66.77 63.60 60.85 Soybean meal. 44% CP 26.06 29.07 32.10 35.10 Mon-Dical—Phos. 21% P 1.12 1.07 1.02 0.96 Ground limestone 1.18 1.19 1.19 1.19 MSU Vit premixh 0.60 0.60 0.60 0.60 MSU TM premixc 0.50 0.50 0.50 0.50 MSU sow packd 0.30 0.30 0.30 0.30 Salt 0.50 0.50 0.50 0.50 ° Diets were formulated using the 1998 NRC requirements for swine. and adjusted for lysine concentration based on litter size. Supplied per kilogram of diet: vitamin A. 5511.49 IU: vitamin D. 551.15 IU: vitamin E. 66 00 IU: vitamin K. 4.40 mg: riboflavin. 4.40 mg: pantothenic acid. 17.60 mg: niacin. 26.40 mg: vitamin Bu. 33.00 ug thiamine. 1.10 mg: vitamin B5. 990 00 ug. Supplied per kilogram of diet: Mn. 11 00 mg: Fe. 11.00 mg: Cu. 11.00 mg: I. 150 ug: Zn. 100 mg: Se. 300 ug. Supplied per kilogram of diet: vitamin A. 2755.75 IU: choline. 385.80 mg: biotin. 220.47 300 pg; folic acid. 1.65 300 pg. 87 Table 4. Composition of diets fed from end of treatment periods through breeding and during gestation (as-fed basis) Diets Ingredient. % Breeding Gestation Corn 75.75 64.64 Wheat bran — 10.00 Soybean meal. 44% CP 17.96 18.55 Mono—Dical-Phos. 21% P 1.74 1.79 Ground limestone 0.82 — Calcium carbonate — 0.99 Choice white grease 2.00 2.00 MSU Vit premixa 0.60 0.60 MSU TM premixb 0.50 0.50 MSU sow packc — 0.30 Salt 0.50 0.50 Antibioticd 0.13 0.13 Supplied per kilogram of diet: vitamin A. 5511.49 IU: vitamin D. 551.15 IU: vitamin E. 66 00 IU: vitamin K. 4.40 mg: riboflavin. 4.40 mg: pantothenic acid. 17.60 mg: niacin. 26 40 mg: vitamin Bu. 33.00 ug thiamine. 1.10 mg: vitamin B6. 990.00 ug. Supplied per kilogram of diet: Mn. 11.00 mg: Fe. 11.00 mg: Cu. 11.00 mg: I. 150 ug: Zn. 100 mg: Se. 300 ug. Supplied per kilogram of diet: vitamin A. 2755.75 IU: choline. 385.80 mg: biotin. 220.47 300 ug: folic acid. 1.65 300 ug. ‘ Tylosin (Tylan®. Elanco Animal Health. Eli Lily & Co.. Indianapolis. IN) supplied at 22.7 mg/kg of diet. >n poo: m pflnfigxo no: can menu mzom No“ voouooou no: mnuumo o» cnzpmn oz magnum co pflnflnxm uoc can pmnp muaflm ho“ umnuooou mn3 >puonsa Lemon 0p manaflom mc—Im" I I .—-I l I l H .I I I N H m m OH m I I m A Homecou mpmpoooz Houpcou mumuoooz Houpcou mumuocoz .mcflcmos pmoa c om n .oom Co a mam >n nmznpmm cu unsung oz mfl00pm>m 00H cQROAm csocxca “oflmmcmnuso can mnpoon mpoamfla noRUMppd Bonumw 0p engaflmm mcoHpAOQ< o>Aoocoo 0p mundaom >ugonsa mcflsoHHoH msupwoc< .>uuonsa gummy 0p whoaflmm wood can poo“ ccsomcD ocflfioovc: canons: commom coefimou cofluflnpsc Hopuoosarmum mauumm an aunnmm 3 0p 0p coflumumoo coflpooaom QNHQHMHNGHU mcoaflmmp coflpflupsc pruonzaroua >n nmocosaucfl mm Ao3pl>ufluma pom mcfiooopn On one mo x3 m Eouuv mcflaaso we mocooflocH .m mannb 89 Table 6. Growth performance of gilts reared using different nutritional regimens from 9 to 25 wk of age D1211 Period‘ Moderate Control SEb Pc n“ 16 16 1 ADG. kg 0.650 0.985 0.024 (0.001 ADFI. kg 1.634 1.718 0.038 0.06 ADG/ADFI 0.336 0.511 0.015 (0.001 2 ADG. kg 1.164 1.118 0.034 0.20 ADFI. kg 2.580 2.437 0.079 0.09 ADG/ADFI 0.426 0.427 0.012 0.92 3 ADG. kg 0.476 0.777 0.034 <0.001 ADFI. kg 2.974 3.145 0.153 0.28 ADG/ADFI 0.173 0.267 0.018 (0.001 4 ADG. kg 1.003 0.726 0.118 0.03 ADFI. kg 3.867 3.381 0.088 (0.001 ADG/ADFI 0.270 0.225 0.041 0.27 Overall' ADG. kg 0.83 0.87 0.03 0.20 ADFI. kg 2.75 2.67 0.05 0.04 ADG/ADFI 0.301 0.358 0.088 (0.001 ° Duration of period 1 was wk 0 to 3. period 2 was wk 4 to 6. period 3 was wk 7 to 11. and period 4 was wk 12 to 16. Standard error of the mean. Probability level. Pen was the experimental unit. Number of gilts per pen varied from four to eleven. Represents average from 9 to 25 wk of age Table 7. Effect of a pre-pubertal feeding regimen on weight. backfat depth (BF). loin-eye area (LEA). and age at puberty E:e_p”bezta| nnrrjtjgn negjmena Moderate Control Pb n 127 120 Moving age. d 187 11.63 187 11.73 0.77 n 125 111 Moving to puberty. d17.3 13.81 18.9 14.06 0.77 Age at puberty. d 203 12.14 205 12.30 0.82 n 112 103 Weight. kg 136.6 11.56 144.1 11.74 0.001 BF.mm 21.78 10.41 21.29 10.39 0.39 LEA.cm2 44.71 10.57 44.08 10.54 0.42 Change in BFZ nmi 15.06 10.41 14.58 10.39 0.39 Change in LEAf. cm2 34.73 10.57 34.12 10.54 0.43 LS means 1 standard error of the mean. Probability level. Represents change from start of experimental nutritional regimen (22.8 kg) to first estrus. 91 Table 8. Effect of a pre-pubertal feeding regimen on pre— lactational (d 110 of gestation) mammary developmenta E _ I | 1 | 'I' Item Moderate Control SEc I>d n 5 5 Total gland weight. g 5087 7296 735 0.10 Right side gland weight. g 2446 3535 344 0.09 Parenchymal weight. g 868 1522 151 0.03 Extraparenchymal weight. g 818 1039 145 0.37 DNA. ug/g' 1011 956 77 0.67 Total DNA. mg 2483 3263 242 0.09 RNA. ug/g' 2907 2654 247 0.54 Total RNA. mg 7116 9435 1167 0.25 RNA/DNA 2.86 2.83 0.25 0.95 Correctedf DNA mg/kg 5.6 4.9 0.50 0.39 RNA mg/kg 16.3 13.5 1.59 0.32 LS means. C Standard error of the mean. D. Probability level. ‘ Per 9 of parenchymal tissue prior to lipid extraction Based on right side mammary glands. Corrected per kg of maternal body weight. Table 9. Effect of a pre—pubertal feeding regimen on sow backfat depth (BF) and loin—eye area (LEA) at breeding and farrowing. lactation feed intake (FI). lactation weight. backfat and loin-eye area change. and wean—to-estrus (WTE) interval Item Moderate Control Pb n 79 52 Breeding age. d 256 14.38 253 15.40 0.67 Weight. kg 153 12.02 150 12.43 0.44 n 74 50 Farrowing age. d 372 14.57 366 15.56 0.40 Weight. kg 185 11.70 187 12.00 0.31 LEA. cm2 40.24 10.63 41.69 10.77 0.15 BF. mm 21.7 10.58 22.8 10.71 0.23 Weaning weight. kg 173 12.93 175 13.32 0.47 LEA. cm2 36.7 10.98 36.7 11.14 0.99 BF. mm 17.4 10.85 19.0 11.00 0.53 Weight change. kg —9.9 12.01 —9.8 12.22 0.95 LEA change. cm2 -2.7 11.03 —3.8 11.1 0.38 BF change. mm —3.6 10.82 —3.1 10.87 0.55 Total FI. kg 101.9 12.84 94.5 13.20 0.02 ADFI. kg n 72 45 WTE. d 9.0 11.15 7.9 11.40 0.42 ° LS means 1 standard error of the mean b Probability level. 93 Table 10. Effect of a pre-pubertal feeding regimen on prolificacy in parity one Era-tntixtil : txit';: ii? i . Item Moderate Control SEb Pc Number born alive 9.75 10.10 0.49 0.50 Stillborn 0.23 0.18 0.17 0.76 Mummies 0.35 0.22 0.15 0.35 Pre—weaning survival% 93.28 90.63 0.02 0.15 b C LS means. Standard error of the mean. Probability level. Table 11. Effect of a pre-pubertal feeding regimen on litter weights (kg) at d 0. 7. 14. and weaning E _ l 1 'l' . . Day Moderate Control Pb n 59 48 0 15.8510.53 16.0210.41 0.79 n 76 48 7 28.6310.50 27.6810.61 0.23 n 75 50 14 47.2610.68 44.8210.82 0.02 n 79 51 Weaning 63.6311.14 61.3511.29 0.07 ° LS means 1 standard error of the mean. ” Probability level. 95 Table 12. Effect of a pre—pubertal feeding regimen on litter gains (kg) between each weigh period at d 0 to 7. 7 to 14. and d 14 to weaning d Era—pnbental nntzjtjgn regimen" Period Moderate Control P” n 57 41 d 0 t0 7 13.3710.80 13.2810.84 0.92 n 72 46 d 7 to 14 19.1110.75 17.0310.83 0.02 n 75 50 d 14 to Weaning 15.2110.68 15.3310.77 0.87 LS means 1 standard error of the mean. Probability level. .006 “0 x3 mm um mcflncm can man “0 as m we mcflccflooo mean mcHHaEmm cum coewmou mcflcoow Happensarmum .H musmflm HImOH no“ woe: mafiaQEmmu h cam peopm 8H 13 HH 13 m 13 13 o 13 am pofiov AD umflov H4 uoHQL Am poHQw 2mmo same game 2mmo cmeamom nonflmlzoq nonflmuzmflx nonflmlsoq nonflmnnmflx ”opnumooz P p _ _ r 1m Swami Ho Swami H< Swami Ia “mama 2mmu 2mmu 2mmo 2mmu coeflmom cmnflma3oq nonamuxoq conflmuzoa 08818-303 “Hooucoo 97 [jModerate gControl 25 20 in H C) H PellnD Z 98 Selection Post breeding Overall Rearing Stage of Culling t 1ng a ll 1ng regimen on cu The effects of a pre—pubertal feed Figure 2. **=P<0.01). 0 O different stages of development (*=P<0.05 .nHo.ovmuxxv ousafiow 0>Hposnonmou one o>HpoEoooH co :oEHmoH mcficoou Hopumnzarmna n “0 muoowuo one .m munmflm GCHHHDU new commmm zonumm o>AmocoU o» ousaflmm o» ousaflom mod coxoum mmmq new Boom Home :00 I my 9360: D 99 PQTTPD X K9 Weight. 140 120 100 , 80 “. 60 ‘0 --O~ Moderate +Control 40 ' a... 20 0 1 . I 0 1 2 3 4 Period Figure 4. The effect of alternating a high-fiber diet with a corn soybean-meal diet on weight during four periods of growth. with the duration of the periods being 3. 3. 5 and 5 wk. respectively (Means at the end of periods 1. 2. 3 and 4 were different at P<0.05). um ng/ml IGF—1. 300.001 +Moderate 250.00~ I ‘\ 200.00 ; K ’ .‘9 ' JI- \ . 1 ‘ L . 1 150.00« ~. __. 100.004 « 'I --l~ Control 50.00 I. 0 00.1 . . . 4 . . . . 1 . , , , 1 2 4 6 8 10 12 14 16 18 Week Figure 5: Changes in IGF—1 concentration pre and post dietary changes during the experimental period. with weeks representing actual sampling time. and occurring 1 wk prior and 1 wk post dietary changes. Diets were changed at end of wk 3. 6. 11. un and 16. APPENDI CBS 102 APPENDIX A Early Weaning Management of Gilts Animal care At 10 d of age (12 d). 206 1 York x % Landrace and 95 % York x % Landrace gilts were weaned into a nursery facility in groups of.10-25 piglets over an eight month period (total of 15 groups). Gilts were housed in 4’x7’ pens. with no greater than seven pigs per pen. At weaning % cc of Procaine G penicillin (Agri Laboratories. LTD.. St. Joseph. MO) was administered in the Trapezius muscle. and gilts were weighed and evaluated for leg and underline soundness. Unsound gilts were were not used for the study. Nursery gilts were allowed ad-libitum access to diet. and water was provided via bowl—nipple waterers. Waterers were allowed to over—flow the first week after weaning. so that they could be easily located and operated by piglets. Room temperature was maintained at about 32°C for the first 2 wks. and gradually decreased 2°C to 3°C per wk with increasing age of the pig. Supplemental zone heat was provided using heat lamps with 125 watt bulbs. Flat 1’ 6 inch x 1' x % inch trays were fastened to the center of each pen. Approximately one cup of feed was placed on the trays daily until pigs had located. and were eating from the feeders (approximately 3 d). NB A series of four different diets was provided during the nursery period (Table 13). Phase one and two were pelleted diets. specifically formulated for this study and manufactured by United Feedsm (Sheridan. IN). Phase one and two were fed until the lightest pig in the pen weighed 4.5 kg and 6.8 kg. respectively. The third and fourth diets were manufactured at Michigan State University and fed in meal form. Pigs were maintained on diet three until the lightest pig weighed 11.4 kg. Diet four was fed until pigs were moved into the grow—finish rooms (63 d 1 7 d: approximately 22.7 kg). Incidence of morbidity and mortality was monitored during the nursery phase and culling was recorded (Table 14). 104 Table 13. Composition of Nursery Diets % Dial Ingredients 1‘ 2° 3” 4” Corn 29.50 40.80 57.64 65.11 Soybean meal.44% CP 15.30 17.88 21.05 27.85 Whey. dried 25.00 20.00 10 00 — Fish meal 6.62 7.50 5.00 — Spray—dried plasma 7.50 2.50 - - Edible grade lactose 7.50 4.00 — - Choice white grease 5.00 4.00 3.00 3.00 Mono-Dical—Phos. 21% P 0.24 0.77 1.35 1.62 Vitamin premixc 0.60 0.60 0.60 0.60 Salt 0.50 0.50 - — Zinc oxided 0.38 0.38 — - Limestone 1.11 0.37 0.63 1.18 Antibiotic' 0.25 0.25 0.25 0.25 Trace mineralf 0.23 0.23 0.23 0.23 Copper sulfates 0.05 0.05 0.10 0.10 L-lysine HCL 78.8% 0.10 0.09 0.15 0.15 DL—methionine 0.13 0.06 — — CalmlateLAnalxz—zis ME. kcal/kg 3429.40 3409.09 3396.40 3408.00 CP% 23.40 21.48 19.64 19.19 Lysine. % 1.70 1.45 1.25 1.15 Met+Cys. % 0.50 0.45 0.36 0.32 Ca% 1.08 0.91 0.90 0.80 P%. available 0.53 0.58 0.54 0. ° Diets 1 and 2 were pelleted diets made at United feeds~(Sheridan. IN). Diets 3 and 4 were meal diets made at Michigan State University. ° Supplied per kilogram of diet: vitamin A. 5512 IU: vitamin D? 551 IU: vitamin E. 66 IU: vitamin K (as menadione sodium bisulfite complex) 4.4 mg: riboflavin. 4.4 mg: pantothenic acid 17.6 mg: niacin. 26.4 mg: vitamin BR. 33 mg: thiamin. 1.10 mg: pyridoxine. 1.0 mg. H5 Table 13 (cont’d) d Supplied 3000 mg of Zn per kilogram of diet (in addition to that provided by trace mineral premix). Supplied 55 mg of carbadox per kilogram of diet. Supplied per kilogram of diet: Zn. 10 mg: Cu. 10 mg: Fe. 100 mg: Mn. 10 mg: I. 0.15 mg: Se. 0.3 mg. Supplied 125mg and 250 mg of Cu per kilogram of diet in diets 1 and 2. respectively (in addition to that provided by trace mineral premix). HM Table 14. Culling of early weaned gilts while in nursery Reason Number of gilts Poor feet and leg structure 2 Abdominal Rupture 1 Compromised Growth” 20 Compromised Health” 14 Deaths 7 Total 44 by 10 wk of age. b 107 Represents pigs that did not reach a weight of 22.6 kg Represents pigs that refused to eat. were losing weight. scouring. or unthrifty. APPENDIX B IGF—1 concentrations Table 15.Plasma IGF—1 concentrations (ng/mL) of gilts before and after dietary changes were made through four different feeding periods E-l|]|" ., Time Moderat Control SE” Pc e n 8 8 Period 1d Preo 58 198 29.61 0.0001 Period 2 Postf 184 182 29.61 0.96 Pre' 225 239 29.61 0.63 Period 3d Post‘ 153 217 29.61 0.03 Pre' 192 135 30.43 0.07 Period 4 Postf 194 145 29.61 0.10 Preo 168 137 29.61 0.30 Final” Postf 202 143 30.43 0.06 ° LS Means. Standard error of the mean. Probability level. Diet contained 35% ground sunflower hulls. One week prior to being switched to diet offered during subsequent period. One week after being switched to diet offered during this period. 9 End of grow-finish period and nutritional regimens. NB APPENDIX C Pre—pubertal feeding regimen and litter size data on sow performance and litter weights Table 16. Effects of pre—pubertal feeding regimen and litter size on changes in sow weight. backfat (BF). loin—eye area (LEA). feed intake(FI). and wean—to—estrus (WTE) from farrowing to weaning Litter Regimen“ Size Item Moderate Control 9 n=16 n=16 Weight Change. kg —6.313.03 -6.513.12 LEA Change. cm2 —0.0211 48 —3.611.53 BF Change. mm —4.311.15 —2 911.22 FI. kg 10014.32 9914.56 MHE. d 8.211.75 7.411.90 10 n=22 n=10 Weight Change. kg —10 612.75 -9.414.12 LEA Change. cm2 —3.711.37 —0.111.99 BF Change. mm -2 811 09 —3.511.59 FI. kg 9614.02 9615.45 WTE. d 8.911.66 9.012.64 11 n=17 n=10 Weight Change. kg -10.613.03 —13.513.77 LEA Change. cmz -4.211.54 -6.211.92 BF Change. mm -2.811.22 -2.611.53 FI. kg 10014.34 8715.50 WTE. d 7.511.92 8.012.34 12 n=15 n=10 Weight Change. kg —11.813 53 —10.713.76 LEA Change. cm2 —5 111.65 —7.811.96 BF Change. mm -4 311.31 —5.611.57 FI. kg 10414.81 9815.50 WTE. d 7 911.94 7 512.23 LS mean 1 standard error H” of the mean. Table 17. Effects of pre—pubertal feeding regimen and litter size on litter weights at d 7. 14. and weaning. and total litter gain between d 7 and weaning Litter Regimen: Size Day Moderate Control 9 7 26 510.94 28 011.09 (12) (16)b 14 43.711.39 43.011.49 (15) (13) Weaning 59.711.75 60.211 84 (16) (16) Gain ' 31.011.53 30.511.51 (14) (15) 10 7 27.410.85 28.211.26 (20) (9) 14 45.011.15 42.011.63 (20) (11) Weaning 62.111 6 58.812.20 (23) (10) Gain 32.511.26 27.711.86 (23) (9) 11 7 31.310 95 28.911.34 (l7) (8) 14 49 511.49 50.311.91 (14) (8) Weaning 63.411 75 64.212.22 (17) (10) Gain 31.911.38 32.611.97 (17) (10) 12 7 33.310.92 31.511.01 (18) (15) 14 55.111 39 51.711.55 (17) (13) Weaning 73.811 89 69 612.22 (16) (12) Gain 38.011.5 36.511.77 (15) (10) LS mean 1 standard error of the mean ” Experimental unit. rm LITERATURE CITED 111 Literature Cited Anugwa. F.O.I.. V.H. Varel. J.S. Dickinson. W.G. Pond. and L.P. Krook. 1989. 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