THE EFFECT OF DiETARY TRIGLYCERiDE CHMN
LENGTH 0N OBESITY EN RATS FED HIGH FAT DIETS

Thesis for the Degree of M. S.
MICHBGAN STATE UNIVERSITY
JOANNE HUSEMAN HNO
1973

   

     
   

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Midzigm State
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ABSTRACT

THE EFFECT OF DIETARY TRIGLYCERIDE CHAIN LENGTH ON
OBESITY IN RATS FED HIGH FAT DIETS

BY

Joanne Huseman Fino

There is evidence in a number of investigations
that medium chain triglycerides<MCT)may not contribute to
the increase in body weight and body fat that is evident
when other forms of fat are fed. (Leveille, §E_§1.,
1967a; Leveille, et_al., 1967b; Harkins and Sarett, 1968b;
Kaunitz and Johnson, 1968; Allee, gE_§l., 1972; Stickney
and Andrews, 1972; Wiley and Leveille, 1973). The
purpose of the present study was to examine some of the
parameters of dietary obesity in rats fed high fat diets
and to compare the effect of substituting medium chain
triglycerides for longer chain fats in these diets. Diets
containing 50% fat as Crisco, corn oil or MCT were fed to

male Osborne—Mendel rats ad libitum, beginning at 21 days

 

of age, for a period of 12 weeks. At the end of the
feeding period six animals from each group were sacrificed

for body composition determinations. The right inguinal,

Joanne Huseman Fino

testicular, and perirenal-retroperitonea1 fat depots were
removed from the remaining six animals, weighed, and uti-
lized for analysis of fatty acid composition.

Total diet consumption by weight in the corn oil-
fed animals was decreased by 5% in comparison to the Crisco-
fed animals. The rats fed the MCT diet ate 5% less grams of
food than the rats fed corn oil. When intakes were adjusted
for digestible Kcal per gram of diet, the gap between the
total Kcal consumption of rats fed the MCT versus the corn
oil and Crisco diets widened. Rats fed MCT consumed 9%
less Kcal than the rats fed corn oil over a 12 week period.

In general, growth rates for the three groups
seemed to reflect the total energy consumed. Rats fed the
Crisco diet attained a final weight of 480 grams while
rats fed corn oil reached a final weight of 454 grams.

Both groups utilized 16.6 Kcal per gram of weight gain.
Rats fed MCT weighed only 369 grams at the end of twelve
weeks and utilized 20.3 Kcal per gram of weight gained.

The greatest difference in body composition was
found in the amount of body fat. The carcasses of the
Crisco and corn oil fed rats contained 27% and 24% fat
respectively. In rats fed MCT only 16% of the carcass

weight was fat. Animals receiving Crisco or corn oil

Joanne Huseman Fino

diets utilized, respectively, 54 and 62 Kcal per gram

of fat gained. MCT fed rats utilized 105 Kcal per gram
of body fat gained. Although the rats fed MCT had
greater lean body mass expressed as a percent of carcass
weight, the total grams of lean body mass found in MCT
rats was significantly less than the values obtained for
the other two groups.

Fat depot weights also varied among the three diet
groups. The decrease in depot weights of the MCT fed
rats was very highly significant when compared to depot
weights in rats fed the other two diets. There was a 33%
decrease in the weights of the inguinal fat depots of the
MCT fed rats compared to the same depots in Crisco fed
rats when fat depot weights were expressed as a percent
of total body weight. There was more than a 50% decrease
between the weights of the testicular and perirenal-
retroperitoneal fat depots of MCT fed rats compared to
the same depots in rats fed Crisco.

Even though 53% of the dietary Kcal were
supplied by C8 and C10 fatty acids, and these fatty acids
were fed during the period of greatest body growth, only
a small increase occurred in these components of adipose

tissue.

THE EFFECT OF DIETARY TRIGLYCERIDE CHAIN LENGTH ON
OBESITY IN RATS FED HIGH FAT DIETS

BY

Joanne Huseman Fino

A THESIS

Submitted to
Michigan State University
in partial fulfillment of the requirements
for the degree of

MASTER OF SCIENCE

Department of Food Science and
Human Nutrition

1973

J... 34 Acmowmncmzms

arr-v"

A special thank you to Dr. Rachel Schemmel, my
academic advisor, whose suggestions, criticisms, and
patient understanding were deeply appreciated during this
work.

A thank you to the members of my committee,

Dr. Charles Sweeley and especially Dr. Gilbert Leveille,
who took time from their busy schedules to assist me
whenever possible.

Thank yous also go out to Dr. Olaf Mickelsen for
obtaining the protein supplement used in the experimental
diets; and to Miss Christine Wierzbicki for her help
during my preliminary gas chromatography work.

Last but not least, thank you to my husband,
Timothy, who endured a part-time wife while she was a

full-time student.

ii

TABLE OF CONTENTS

ACMOWLEDGMENTS O O O O O O 0

LIST

LIST

I.

II.

III.

IV.

OF TABLES . . . . . . .
OF FIGURES . . . . . .
REVIEW OF LITERATURE . .
Fat: Boon or Bane .

Determination of Obesity
Etiology of Obesity . .

Theories of Appetite Control

'Genetic Factors in Obesity
Inactivity . .
Psychology of Obesity .
Treatment of Obesity .

Medium Chain Triglycerides: A Review

Nutritional Studies . .

Physical- -Chemical Properties

Gastric Retention .
Hydrolysis and Absorption
Liver Metabolism . .
Adipose Tissue Metabolism
Plasma . . . . . .
Clinical Applications .

INTRODUCTION . . . . . .

METHODS O O O O O O 0

Selection and Care of Animals
Diet . . .
Body Composition Analyses .

Fat Depot Weights, Total Triglyceride

and Fatty Acid Composition .
Statistical Analysis . . .

RESULTS AND DISCUSSION . .
Diet and Kcal Consumption
Growth Rates . . . .
Body Composition . . .
Fat Depot Weights . .
Fat Depot Triglyceride Content

iii

Page

ii

vii

Fat Depot Fatty Acid Composition .

Plasma Free Fatty Acids and Triglycerides
Food Preference

Fat Digestibility .

SUGGESTION FOR FURTHER STUDY

Fat Soluble Vitamin Absorption.

Effects on Human Obesity

v.
VI. CONCLUSIONS
BIBLIOGRAPHY. .

iv

Page

51

52
52
52
52
53
53

55

69

Table

1.

4a.

5a.

6a.

LIST OF TABLES

Composition of Rations . . . . . . .

Fatty acid composition of Crisco, corn
oil, and MCT. (Values are expressed as
percentage of the total fatty acids in
the fat) . . . . . . . . . . . .

Fatty acid composition of Crisco, corn

oil, and MCT diets. (Values are expressed
as percentage of the total fatty acids in
each diet) . . . . . . . . . . .

Dietary intake of male Osborne - Mendel

rats fed high fat diets containing Crisco,
corn oil, or MCT for 12 weeks; and conversion
factors for determing energy and Kcal:
protein ratio in the rations . . . . .

Scheffe confidence intervals (0.975) for all
possible contrasts of mean differences in
total diet consumption and total Kcal
consumption . . . . . . . . . . .

Absolute body composition of Osborne-Mendel
male rats fed high fat diets containing
Crisco, corn oil, or MCT for 12 weeks . .

Scheffe confidence intervals (0.975) for all
possible contrasts of mean differences in
body composition (grams), . . . . . .

Relative body composition of Osborne-
Mendel male rats fed high fat diets con-
taining Crisco, corn oil, or MCT for 12
weeks . . . . . . . . . . . .

Scheffé confidence intervals (0.975) for all
possible contrasts of mean differences in
body composition (%) . . . . . . . .

Page

57

58

59

60

6O

62

62

63

63

Table
70

7a.

8a.

10.

11.

12.

Relative inguinal, testicular, and
perirenal—retroperitoneal fat depot
weights of Osborne-Mendel male rats fed
high fat diets containing Crisco, corn

oil, or MCT for 12 weeks. . . . . . .

Scheffe confidence intervals (0.975) for all
possible contrasts of mean differences in
fat depot weights (grams) . . . . . .

Relative weight of triglyceride in
inguinal, testicular, and perirenal-
retroperitoneal fat depots of male Osborne-
Mendel rats fed high fat diets containing
Crisco, corn oil, or MCT for 12 weeks . .

Scheffe confidence intervals (0.975) for
all possible contrasts of mean differences
of relative weight of triglyceride in fat
depots . . . . . . . . . . . .

Mean fatty acid composition of inguinal

fat depot of male Osborne-Mendel rats fed
high fat diets containing Crisco, corn oil,
or MCT. Values are expressed as percent
of total fatty acids . . . . . . . .

Simple correlation coefficients for
initial weight, food intake, calorie
intake, diet and final weight . . . . .

Simple correlation coefficients for
initial weight, food intake, (cal
intake, diet and final weight . . . . .
Simple correlation coefficients for initial
weight, food intake, Kcal intake, diet,
final weight and percent body composition .

Simple correlation coefficients for
initial weight, food intake, Kcal

intake, diet, final weight, and weight of
the inguinal (ing), testicular (test), and
perirenal—retroperitoneal (peri) fat
depots . . . . . . .

vi

Page

64

64

65

65

66

67

67

68

Figure

1.

LIST OF FIGURES

Mean growth rates of male Osborne-
Mendel rats fed high fat diets containing
Crisco, corn oil or MCT for 12 weeks from
the time of weaning at 21 days of age.

vii

Page

61

REVIEW OF LITERATURE

Fat: Boon or Bane

 

The ability to store lipid is an adaptive feature
of animals which has had considerable survival value.
The seasonal lipid stores of migratory birds is only
one example of adaptive obesity which allows these small
mammals to store enough energy to carry them half across
the globe. In the hummingbird, for example, the normal
body fat content of 3—10% can increase to 45% within days
due to hyperphagia immediately preceding migration (King
and Farner, 1965). This fat content exceeds levels
normally considered pathological in most animals.

Fat in the form of triglycerides is an ideal
storage form of energy for mobile organisms. It has a
relatively low density and yet it is high in energy value.
'Senior (1964) pointed out that even though triglycerides
seem to require a number of hydrolysis and resynthesis
cycles to be moved across membranes, one cycle of
hydrolysis and resynthesis costs only 0.7% of the energy
metabolically available from fatty acid oxidation. The

hydrolysis and synthesis cycles also permit the organism

to synthesize preferred forms of lipids and to arrange
them in suitable configuration. Thus fat is a very
unique and necessary component of animal bodies.

The ability to store fat ceases to be an asset
and becomes a liability when food is plentiful and
strenuous exertion become unnecessary. Americans, in
general, have found that the ability to store fat has
become a liability in their affluent society. It is
estimated that weight control is a major nutritional
concern of 20 to 40 million Americans (Wagner, 1970).
Obesity is becoming a greater problem in the well-fed,
technical societies all over the world. Not only a
problem from a cosmetic point of view, obesity has been
associated with increased risk of death from cardiovascular
and renal disease, diabetes mellitus, cirrhosis of the

liver in men, appendicitis, and gallstones (Baird, 1969).

Determination of Obesity

 

Another major problem associated with obesity is
determining who is obese. If obesity is defined as an
excess of body fat, then some method of estimating body
fat must be used in the diagnosis. Standard height and
weight charts are useful, but subjects may have excess

adipose tissue and still be normal weight while athletes

may be overweight due to an excess of lean body mass
rather than fat. Using hereditary obese mice Alonso and
Maren (1955) found that if food intake was restricted
so that the obese mice were the same weight as lean
controls, the obese mice still possessed an increased
amount of body fat. As the weight of lean and obese
individuals increased, the obese mice deposited more fat
per unit weight gain than the lean controls. Thus body
weight per se is a poor indicator of obesity.

A number of standardized definitions of obesity
have been proposed (Lebon, 1969). The most common being
a body weight which is 20 to 30% above ideal body weight.

Others, which try to be more discriminating, include

 

having a Ponderal Index (ht. in inches 3wt. in lbs.)

less than 12 or having a fat fold thickness greater than
2.5 cm. as measured at the tip of the scapula in man or

at the mid triceps region in women. All of these formulae
try to approximate total body fat; a difficult measure-
ment to obtain in human subjects. Behnke (1952, 1964)
listed other techniques which have been used for deter-
mining body composition in live subjects, including meta-
bolic balance studies, roentgen visualization, densio-

metry, isotope dilution, measurements of exchangeable

electrolytes and gamma emission of K40. Small animal

body composition determinations do not present the pro-
blems encountered in the determination of body composition
in human subjects. Direct analysis can be performed on

the animal after sacrifice (Mickelsen and Anderson, 1959).

Etiology of Obesity

 

The etiology of obesity cannot simply be stated
as availability of food and lack of exercise. Although
obesity is an ever growing problem in affluent societies
the majority of Americans still manage to remain within
the norms for body weight. Obesity is caused by more
than one factor. Errors in appetite regulation, genetic
predispositions and environmental stress, inactivity, as
well as psychological disorders have all been implicated

as factors in the development of obesity.

Theories of Appetite Control

 

The theory that "energy in" equals "energy out"
is a basic one to all sciences. The definition of simple
obesity given in Swift and French (1954) is in terms of an
imbalance in food intake and energy expenditure. Factors
influencing food intake seem to have received more

attention than energy expenditure and a number of theories

of the mechanism of food intake regulation have appeared.

Brobeck (1946) reported that lesions of the
hypothalamus produced rapid weight gain in animals.
Animals so lesioned often increased their body weight by
15% within 24 hours and continued to gain weight at rates
10 times that of normal animals until a plateau was finally
reached. Although there was an indication that these
animals were less active than normal and their basal
heat production could have been altered, Brobeck attributed
the obesity in these animals to their marked hyperphagia.
This was one of the first indications that some sort of
appetite regulation camnzed in the intact hypothalamus.
Since then a number of possible theories have been pro-
posed as to the mechanism of hypothalamic regulation of
appetite.

Brobeck has proposed a temperature regulation of
appetite. In a discussion of this theory (Brobeck, 1955),
he stated that body weight itself may not be regulated
although food intake, heat loss and activity are directly
controlled. Because heat loss is under stricter metabolic
controls than either food intake or activity the latter

two are changed in relation to the former.

Mayer has proposed a glucostatic regulation of
food intake. In a review of this theory (Mayer, 1957)
it was stated that the rate of glucose passage in cells
of the ventromedial hypothalamus controls food intake.
In support of this theory is the fact that goldthioglucose
but no other goldthio compounds can selectively destroy
the hypothalamus.

Kennedy (1953) found little connection between
the hypothalamic center and temperature regulation, but
rather, he postulated that it was lipemia which influence
food intake. Wide variations in diet composition had
little effect on food intake in normal rats suggesting
glucose alone could not be the appetite regulator. The
limit of food intake was a function of maximal fat ass1-
milation. Other support for this theory came from
Liebelt, et_gl, (1965) who found that there was a
"compensatory hypertrophy" of other fat depots when the
gonadal depot was removed, suggesting that the adipose
tissue itself feeds back to a food intake regulator.

The fact that appetite is well controlled in the
normal animal is illustrated in an experiment in which
Janowitz and Hollander (1955) varied the intragastric
feeding of dogs and recorded their adjustments in oral

intake and body weight. Gastric distension was kept

constant and caloric density of the intragastric feeding
was varied at 50%, 100% and 175% of the average oral intake
of each dog. After the intragastric feeding the dogs

were allowed access to food orally. Within five weeks of

a change in density of the intragastric feeding, the dogs
had adjusted their total food consumption to levels

which maintained body weight constant with the 50% feed-
ing, or in the case of the 100% and 150% levels, oral
intake drOpped to almost nothing.

In a study in rats, Kennedy (1950) reported that
normal animals regulated food intake within one week after
their diet was adulterated with 50% Kaolin. In the same
experiment, hypothalamically lesioned animals required 4
weeks to regulate their food intake and lost considerable
weight during this period.

A most interesting study was performed by Hashim
and Van Itallie (1965) in which human subjects were asked
to consume their total food intake from a specially
designed dispensing device. The device recorded the
amounts of a liquid diet consumed and the only way the
subject could estimate the amount of food eaten was by
the number of mouthfuls. Normal weight subjects had
little problem regulating intake and maintaining normal

weight. Obese subjects, on the other hand, could not

regulate intake and consistently lost weight when fed in
this manner. Thus obese human subjects seem to exhibit
some of the difficulty regulating food intake seen in rats
with hypothalamic lesions. That the hypothalamus is
involved with appetite regulation is clear. But as yet
the precise mechanism of control, whether glucose, free

fatty acids, or temperature is unclear.

Genetic Factors in Obesity

 

There is a strong correlation between overweight
in parents and overweight in their children. Studies
have shown that about 10% of children from families of
normal weight parents eventually become obese, while 50%
of children from families with one obese parent and 80%
of children from families with two obese parents become
obese (Mayer, 1957, 1965a). Eighty percent of overweight
children remain overweight in adulthood (Lloyd, 1969).
These data are not conlcusive proof that obesity is
hereditary as it is impossible to separate the influence
of the home environment in each of these cases.

Mayer (1965a) reviewed a study of identical and
fraternal twins and their siblings. There was a definite
correlation between weight in identical twins that was

absent between fraternal twins or when the twins were

compared with their siblings. It was also repOrted that
sex ratios of offspring were altered when obese x obese,
obese x lean, or lean x lean parental unions were com-
pared; thus suggesting a sex linked inheritance pattern
for obesity. Body weights of children correlated well
with those of their natural parents but when adOpted chil-
dren were examined, there was no correlation between the
body weights of the child and those of their adoptive
parents.

Animal studies have been helpful in examining
the genetic aspects of obesity. The ability to select
animals with characteristics under study and breed for
the phenotypic expression of these characteristics gives
these studies an experimental design unavailable with
human subjects. A number of genetic obesities have been
isolated in rats and mice. The Zucker rat contains a
recessive gene producing spontaneous obesity in animals
homozygous for this gene (Zucker, 1965). There are at
least four different strains of obese hyperglycemic mice
in which the obesity is again a recessive trait expressed
in animals homozygous for this trait (Hellman, 1965;
Stauffacher, et_al., 1965). Even in apparently normal
strains of rats it has been possible to selectively breed

high and low weight animals until distinctive substrains

-10

have been develoPed differing in food efficiency, body
composition, as well as body weight (Palmer, et_§1., 1946;
Kleiber and Cole, 1950).

By examining the metabolic aberrations in geneti-
cally obese animals it may be possible to identify similar
metabolic changes in human obesity. Bray (1970) reported
on a comparison of obesity in the Zucker obese rats, lean
controls, and lean controls with hypothalamic lesions.

The Zucker rat and lesioned control reached final body
weights 2 times that of the normal control and their

food intake was almost 50% greater per day than that of
the normal control. Other differences found were a
decrease in liver glycogen in the two obese groups, and
substantially higher circulating insulin and triglyceride
levels. One characteristic of interest that was possessed
by the Zucker rat and not by the lesioned control was a
slower turnover of radioactive iodine, possibly indicating
groups of obese animals were pair fed with controls the
Zucker obese rat gained weight more rapidly than the
normal or the lesioned control animals. Thus even though
the Zucker and hypothalamically lesioned rats had

increased ad libitum food intakes there seemed to be other

 

factors contributing to the genetic obesity. Bray also

11

reported that in human obese subjects there were abnormally
low levels of HAD-linked glyCerophosphate dehydrogenaSe

and mitochondrial glycerophosphate dehydrogenase. Low
levels of these two enzymes seemed inconsistent with the
known increase in lipogenesis in obesity but Bray pro-
posed that a decreased activity of the glycerophosphate
dehydrogenase cycle could increase the efficiency of
oxidative phosphorylation.

Stauffacer, gt_al. (1965) examined some differences
in glucose utilization between obese hyperglycemic mice
and lean controls. Both groups were of identical body
weight although the obese hyperglycemic mice had an
increased amount of body fat. The obese hyperglycemic
mice exhibited a decreased incorporation of glucose into
diaphragm glycogen and an increased incorporation of
glucose into adipose tissue at l and 2 months of age.

By three months of age the lean controls also had more
glucose incorporated into adipose tissue than into
diaphragm glycogen.

Besides spontaneous genetic obesity, there is
indication that rats and mice may inherit a susceptibility
to obesity if placed in nutritionally stressful conditions.
Fenton and Dowling (1953) showed that in 2 strains of mice

studied, high fat diets (43% fat w/w) produced more rapid.

12

weight gains than low fat diets. But in one strain diets
containing more than 15% fat actually inhibited weight
gain. Schemmel, gt_§l. (1970a) also found a difference in
weight gain and body composition in seven strains of rats
fed a low fat grain diet compared to a 60% (w/w) fat diet.
Hypothalamic lesioning has been said to produce
a regulatory obesity as the obesity seems to be caused
by simple hyperphagia (Mayer, 1957). Genetic obesities
have been termed "metabolic" as they seem to be connected
with an inborn error in tissue metabolism (Mayer, 1957).
Both models have counterparts in human obesity and both
models are being used to examine the complexities of

obesity in man.

Inactivity

 

The traditional view of an obese person as a
lazy glutton is based on the laws of thermodynamics,
energy intake will equal the energy stored plus "energy
output." Mayer (1965b) reported that studies of activity
levels in obese adolescent girls showed a 2/3 reduction
in activity when they were compared to lean peers.
Brobeck (1946) also commented on the lethargy reported
in obese animals with hypothalamic lesions. Although it

is safe to say that inactivity in these two cases

13

undoubtedly contributed to the maintenance of obesity;
it cannot be ascertained whether inactivity is truly a

cause or an effect of obesity.

Psychology of Obesity

In man, the metabolic and physiological aspects
of obesity are compounded by the emotional. .As Hamburger
(1957) states, man has the "non-nutritional" aspect of
eating for which to account. Adult appetite is a learned
psychological experience associated with love, companion-
ship, religion and all other areas in which food plays
a role in society. Miller (1955) expressed the view
that hunger cannot be measured by food consumption alone,
even in animals. Food consumption is regulated more by
a balance of hunger and satiety. Rats with hypothalamic
lesions will consume larger amounts of readily available
food but they will not work to secure food not readily
available. Thus even in lesioned rats, they ate more but
were less "hungry" than normals. Monello, et_§l. (1965)
found abnormalities in satiety much more prevalent than
abnormal hunger in obese subjects. While non obese
women associated feelings of hunger with gastric
mobility, Stunkard (1959) found that obese women rarely

reported hunger at all even though their periods of

14

gastric mobility were similar. Hashim and Van Itallie
(1965) reported consistant weight loss in obese subjects
fed a liquid diet from a feeding machine where the
subjects could not see the food or the amount they were
consuming.

Although there is no one psychological profile
for the obese person there are a number of common
psychological problems among the obese. Stunkard and
Mendelson (1967) reported a common disturbance of obese
subjects was related to body image. The earlier the age
of onset of obesity; the more negative the evaluation of
their obesity by others; and the presence of other
emotional disturbances; tended to create problems, not
only in the obese persons' view of themself, but also
in their view of others. Bruch (1955) reported that the
obese tended to have great fear of starvation. Stunkard
(1955, 1957) also warned of the emotional dangers of
dieting which could cause severe anxiety and depression
in some patients.

It is still not clear how the obese persons'
altered feelings of satiety or hunger, their altered
response to sensual cues or their disturbed image of

themselves and others contributes to the develOpment or

15

maintenance of their obesity. One aspect is clear,
however. The psychological aspects of obesity can only

be elucidated by man studying man.

Treatment of Obesity

 

Again science had looked at a simple energy
equation and come to the conclusion that to treat obesity
one merely had to cut down energy intake or increase
energy output. So reducing diets and exercise clubs
were born. Maybe it was indicative of the failure of
those two prescriptions that other techniques were tried.
Total fasting (Duncan, §E_§l., 1965), bowel by-pass
(Sherman, et_al., 1965), alterations in dietary com—
position (Kekwick and Pawan, 1956) and alterations in
meal frequency (Young, gt_al., 1971; Leveille, 1972)
are only some of the treatments that have been used in
combating obesity. The relative ineffectiveness of mOst
weight reduction programs is reflected in the statistics
from Jordan (1973) which stated that attrition rates in
clinics range from 20 to 80% of those treated. Only
25% of those who begin therapy lose as much as 20 lbs.
and only 5% lose as much as 40 lbs.

Perhaps one aspect of the high rate of failure
of weight reduction therapy is due to the total re—educa—

tion towards food required in patients. A total break

16

with old eating habits is necessary. But rather than a
total change from a familiar diet perhaps a slight
remodeling would be more effective.

The average American obtains about 40% of his k110—
calories from fat (Pike, 1967). It had been reported that
high fat diets can cause obesity in mice and rats (Fenton
and Dowling, 1953; Schemmel,‘g§+al., 1970a). If dietary
fat is a factor in human abesity it may well be wise
to investigate substitutes for conventional fats, without
their high predisposition toward obesity, and yet able to
provide the satiety value and to provide the cooling

properties of fat.

Medium Chain Triglycerides: A Review

 

Progress in the understanding of triglyceride
absorption and metabolism has occurred at an impressive
pace in the past 30 years. In these investigations it
was recognized that all natural fats were not equivalent
in chemical or physiological properties. Steinbock, gE_§l.
(1936) compared the absorption rates of different fats
and found that butter fat exhibited a very rapid initial
absorption rate. The shorter, somewhat water soluble
fatty acids contained in butter were more rapidly absorbed

than the longer chain fatty acids. It became increasingly

l7

apparent that fatty acid chain length was an important
variable in triglyceride metabolism.
Long chain fatty acids are the most prevalent

).

fatty acids in natural triglycerides. Stearic (C18°0

oleic (C ), linoleic (C ), and the higher chain

18:1 18:2
polyenoic fatty acids constitute the majority of
naturally occurring fatty acids. Only 5% of naturally
occurring fatty acids have carbon chains of less than
fourteen (Hashim, 1967). These medium chain fatty acids
(MCFA) are found to a small extent in milks and more
extensively in kernel oils (Babayan, 1968). Medium chain
triglycerides (MCT) are a synthetic oil composed of a
random mixture of these saturated fatty acids, eight to
ten carbons in length. This review will try to examine

some of the unique absorptive and nutritional properties

Of MCT.

Nutritional Studies

 

Medium chain triglycerides differ from long chain
triglycerides in caloric value. Naturally occurring fats
have a caloric value of 9.2 Kcal per gram. MCT yields
8.3 Kcal per gram by bomb calorimetry (Kaunitz, gt_al.,
1958).

Nutritional studies of MCT have been conducted

using 10-33% (w/w) of the diet as medium chain or long

18

chain fats. While Kaunitz, §E_§l. (1958) reported
slightly higher food intakes on MCT diets, wiley and
Leveille (1973) reported a 5% decrease in food
intake in rats consuming MCT when compared to diets
containing corn oil or lard. Most investigations agree
that MCT-fed animals tend to be lighter in weight than
animals fed longer chain fats (Leveille, gt_§1., 1967;
Leveille, et_§1., 1967b; Harkins and Sarett, 1968b;
Kaunitz and Johnson, 1968; Allee, §E_§1., 1972; Stickney
and Andrews, 1972; Wiley and Leveille, in press). By
restricted feeding, weight maintenance requirements were
found to be higher for MCT diets than for lard diets
(Kaunitz, gt_31., 1958), and higher than for fat free
diets (Kaunitz and Johnson, 1968). The poor growth rates
of rats on MCT diets was not related to poor utilization
of the fat, as MCT absorption is rapid and more complete
than that of long chain fats (Bloom, gt_§l., 1951). Fecal
fat losses in rats consuming MCT were found to be slightly
lower than those observed for rats consuming longer chain
triglycerides (Kaunitz, et_al., 1958; Kaunitz and Johnson,
1968; Harkins and Sarett, 1968b).

In studies of carcass composition, rats fed 20%
MCT were found to have slightly less carcass fat than rats

fed other types of fat (Harkins and Sarett, 1968b).

l9

CatfiSh fed a 10% MCT diet did not show an increase in
carcass lipid above those fed a low fat control diet
(Stickney and Andrews, 1972). Harkins and Sarett (1968b)
reported a decrease in epididymal fat depot weight in

rats fed 20% MCT as opposed to rats fed 20% corn oil.

Physical-Chemical Pr0perties

The physical-chemical properties of medium chain
fatty acids are distinct from those of longer chain
conventional fatty acids. Medium chain fatty acids exhibit
a greater solubility in water; 68 mg/100 ml at 20°C for
octanoate as compared to 0.7 mg/100 ml at 20°C for
palmitate (Harkins and Sarett, 1968a). The melting point
of octanoate is 17°C while that of palmitate is 63°C
(Ibid). The most important distinction though, is the
manner in which medium chain fatty acids and their

triglycerides are metabolized.

Gastric Retention

 

Gastric retention is influenced by a number of
factors not well understood. It is well known, though,
that dietary fat tends to increase gastric retention,
presumably by influencing the release of an inhibitor of

gastric motility from the duodenum (Wiseman, 1964). In

20

a comparison of the gastric retention of liquid diets
containing different fats, a diet containing 4-8% MCT
was found to decrease gastric retention of fat when
compared to similar levels of longer chain triglycerides
(Harkins, et_al., 1964). There was no evidence of a
selective emptying of the stomach which could have

favored evacuation of shorter chain fatty acids.

Hydrolysis and Absorption

 

Fats are hydrolyzed and absorbed in the small
intestine. Hydrolysis depends on bile salts and pancreatic
lipase. Medium chain triglycerides are hydrolyzed much
more rapidly than long chain triglycerides both in vitro
and in vivo (Greenberger, gt_al., 1966; Hagerman, et_§1.,
1969). The absence of bile has little effect on MCT
hydrolysis; and even in the absence of pancreatic lipase
some absorption of medium chain fatty acids does occur
(Greenberger, et_al., 1966; Isselbacher, 1968; Clark,

1968; Hagerman, et_al.,'l969). An examination of normal
intestinal hydrolysis products of trioctanoin and

tripalmitin showed more free fatty acids were produced from
the trioctanoin and more lower glycerides, especially
monoglycerides were produced from the tripalmitin (Green-
berger, et_al., 1966). This could possibly reflect the
greater importance of monoglycerides in the dispersion of long
chain hydrOphobic fats. Medium chain triglycerides are

much less hydrOphobic in solution than are long chain

21

triglycerides. Hoffman (1968) explains the increased
rate of MCT hydrolysis and its independence of bile
concentrations by the fact that MCT is dispersed in water
and in water-bile salt solution at 370C. Long chain
triglycerides are not dispersed in either of these systems.
Hoffman proposed that MCT is more rapidly hydrolyzed by
pancreatic lipase because of its dispersion in the
intestinal lumen. Desnuelle and Lavary (1963) believe
that it is the water-lipid interface that is important
for lipase activity. The hypothesis being that the lipase
must be absorbed at this interface to be active. Although
precise Km values are lacking for the reactions catalyzed
by lipases it seems as if there is a preferential
hydrolysis of shorter chain fatty acids. Whether this
is a function of the larger interface of a more dispersed
water-lipid system, or a function of chain length
specificity of the lipase reaction has not yet been
answered.

In absorption studies it was found that MCT was
not absorbed into the lymph as were long chain fats, but
rather medium chain fatty acids were absorbed as free
fatty acids directly into the portal vein (Borgstrom,
1955; Bloom, gt_al., 1964; Hashim, et_§l., 1964).
Intestinal acyl CoA synthetase activates shorter chain
fatty acids very slowly (Desnuelle and Lavary, 1963).

It was postulated that the specificity of the synthetase

22

determined which fatty acids were esterified in the
mucosa and packaged as chylomicrons for transport in the
lymph. The medium chain fatty acids were not readily
esterified and were thus destined for portal transport
to the liver.

Other evidence indicates that triglycerides
may be able to enter the portal system. Greenberger,
gt_gl, (1966) injected trioctanoin - l4Ceinto normal
and irrigated intestinal loops. .After 15 minutes the
portal blood from the normal loOp contained 40.3 x 10-3
dpm/ml; 83% of the label was in the form of free fatty
acid and 16% of the label was neutral lipid. In the
case of irrigated 100ps, portal blood label was reduced
to 3.8 x 10-3 dpm/ml of which 74% was neutral lipid.
Thus, impaired intraluminal hydrolysis of MCT was able to
alter the lipid profile of portal blood.

A lipase associated with intestinal cell
microsomes and which hydrolyzes trioctanoin but not
tripalmitin was described by Playoust and Isselbacher
(1964). Even when bile and pancreatic lipase are
unavailable intraluminally, the mucosa has a small
capacity to hydrolyze absorbed medium chain tri-and lower
glycerides. Also, the activity of a MCT-specific
lipase and a LCT—specific CoA synthetase favors the
formation of free medium chain fatty acids for portal

transport.

23

During MCT absorption there is less chylomicron
formation and a slight decrease in intestinal lymph
flow. The proportion of medium chain triglycerides in
the diet in relation to long chain triglycerides
influences the incorporatiOn of medium chain triglycerides
into chylomicrons. Using tripelargonin, Lee, et_al.
(1968) found less than 1% of an oral dose was absorbed
into the lymphatic system. As the percentage of long
chain triglyceride in the dosage increased, the per-
centage of MCT found in chyle triglycerides increased.
It was not determined whether the MCFA in the chyle
were due to an incorporation of these fatty acids into
mixed triglycerides with long chain fatty acids. Sylven
(1970) found that when MCT was found in the lymph,
it was contained in a lower density chylomicron which
had a higher amount of cholesterol and lowered triglyceride
content. While dietary long chain triglycerides can
influence MCT transport, dietary MCT may influence long
chain triglyceride absorption. Clark and Holt (1969)
demonstrated a 68% inhibition of triolein absorption
when intestinal infusion of trioctanoin was maximal.

Harkins and Sarett (1968b) investigated the
relationship of fat absorption to protein and calcium

absorption in the rat. Fecal excretion of MCT was

24

decreased below the average levels of five other fats
examined, but little difference was seen in the protein

or calcium excretion levels for the different diets.

Liver Metabolism

 

Scheig and Klatskin (1968) compared the hepatic
metabolism of 1-14C—octanoate and 1—14C-palmitate in the
rat. In vivo studies showed that octanoate produced
more water soluble products and less lipid soluble
products; while in vitro investigations showed that
labeled CO2 production was greatly increased by octanoate.
Examination of incorporation into liver lipids showed
that about 50% of both medium and long chain fatty acids
were found in the triglyceride fraction, but labeled
octanoate was found to a greater extent in unesterified
fatty acids and less in the phospholipid fraction when
compared to palmitate. Harkins and Sarett (1968b)
reported a slight decrease in total liver lipids and
cholesterol and an increase in liver phospholipids in
rats that had been fed a diet containing MCT. Earlier,
Leveille, et_al. (1967a; 1967b) had shown in rats and
in chicks, the effect of MCT on liver cholesterol levels
was a function of changes in the liver—plasma cholesterol

pool and was influenced by dietary cholesterol levels.

25

In rats fed a diet without cholesterol, liver fat and
cholesterol decreased only slightly while a large
decrease in plasma cholesterol lowered the total pool
size considerably. Chicks responded to cholesterol-free
diets in the opposite manner. The decrease in liver
cholesterol observed in chicks was offset by an increase
in plasma cholesterol and pool size remained the same.
In both species cholesterol-supplemented MCT diets
lowered liver fat and cholesterol with little or no
effect on plasma levels. Increases in the liver's
ability to lengthen fatty acid chains was reported in
the chick and in the rat (Levelille, et_al., 1967a;
Levelille, et_al., 1967b; Scheig and Klatskin, 1968). In
yitrg studies in the chick had shown that MCT feeding

increased acetate-l-14C incorporation into CO fatty

2,
acids and cholesterol (Leveille, et_al,, 1967b). Rat
liver showed a decreased incorporation of labeled acetate
into cholesterol and no change in acetate incorporation
into fatty acid after MCT feeding (Leveille, et_§l.,
1967a). In vitro studies of fatty acid synthesis from
glucose indicated an increase in liver synthesis of fatty

acids (Wiley and Leveille, 1973). Enzyme actiVities

of glucose-6-phospate dehydrogenase plus 6—phosphogluconate

26

dehydrogenase were increased after MCT feeding although
citrate cleavage enzyme and malic enzyme were depressed
to a similar extent when compared to levels in livers
from lard or coconut oil fed rats.

Lieber, e£_al. (1967) found that MCT reduced the
increase in hepatic triglycerides seen in diets high in
ethanol. The same investigators found that alcohol in

the profusion media decreased rat liver CO production

2
from labeled chylomicrons or free fatty acids. When the
products of the free fatty acid metabolism were compared,
almost all of the palmitate-14C label occurred in hepatic
lipids while the octanoate-14C label was found primarily
in C02. Alcohol in the profusion media increased the
amount of both free fatty acids incorporated into hepatic
lipids but in no case did octanoate incorporation into

hepatic triglycerides exceed 40% of the total label

recovered.

Adipose Tissue Metabolism

 

There is little deposition of medium chain fatty
acids in adipose tissue although there is a shift toward
increased palmitate and a decrease in tissue linoleate
levels (Leveille, et_§l., 1967a; Harkins and Sarett,

1968b; Kaunitz and Johnson, 1968; Tamir, et al., 1969).

27

This is understandable in view of the rapid hepatic
metabolism of medium chain fatty acids previously dis-
cussed. The only significant enrichment of depot fat

with medium chain fatty acids was reported by Zurier,
'§t_al. (1967). By shunting the portal venous blood
directly into the systemic circulation the levels of
labeled perlargonin were increased in omental fat depots
from zero to 12.4% in one month of feeding a diet in which
tripelargonin supplied 30% of the total Kcal. Sham-
,operated control rats fed the same diet showed only a 3.9%
increase in adipose tissue pelargonin. An interesting
aspect of this study was the fact that octanoate was not
incorporated into adipose tissue to the extent that
pelargonin was incorporated; neither after feeding nor after
the portal-systemic shunt. Devi, gt_§l. (1969) examined
the effect of small and medium chain fatty acids on
glucose uptake in rat epididymal adipose tissues and

found that only pelargonin (nonanoate) significantly
increased glucose uptake by the tissue. Thus it seems as
if the odd-carbon chain C9:0 fatty acid is more readily
incorporated into tissue lipids when compared to the even-
chain C8:0 or C10:0 fatty acids even though the tripel-
argonin is not normally a component of the tissues or the

diet.

28

Fatty acid synthesis is increased in MCT feeding
similar to the increase seen in low fat-high carbohydrate
diets both in the rat and in the pig (Leveille, et_al.,
1967a; Allee, et_al., 1972; Wiley and Leveille, 1973).
Although there is a small increase in the conversion of
acetate to CO in adipose tissue of rats fed MCT, pigs do

2
not show an increase in CO2 production from acetate. In
the pig the activities of malic enzyme and citrate
cleavage enzyme are increased, while in the rat only
increases in glucose-6-phosphate dehydrogenase and 6-

phosphogluconate dehydrogenase could be found in adipose

tissue.

Plasma

The levels of a number of_p1asma constituents are
changed in MCT feeding. As was mentioned previously, in
the rat, MCT-cholesterol—free diets decrease plasma
cholesterol, while in the chicken there is little change in
plasma cholesterol levels with MCT-cholesterol-free or MCT-
cholesterol-supplemented diets (Kaunitz, et_al., 1958;
Leveille, et_al., 1967a; Leveille, et_al., 1967b; Harkins
and Sarett, 1968b). Total plasma lipids are decreased in
the rat with MCT feeding (Leveille, gt_al., 1967a; Wiley

and Leveille, 1973). In the pig, Allee, et a1. (1972)

29

found plasma cholesterol, free fatty acids, as well as
plasma glucose decreased in animals fed MCT. Children fed
MCT in the treatment of malabsorption were found to have
lower plasma cholesterol and slightly elevated
triglyceride levels (Tamir, et_al,, 1969). MCT diets
greatly increased blood ketones in the pig and in the rat
reflecting their rapid metabolism in the liver. (Allee,
gE_§l., 1972; Wiley and Leveille, 1973). In a study

of the effect of MCT in meal-fed rats, Theuer (1971)

found that the glucose levels were decreased, the levels
of non-esterified fatty acids were increased, and ketones,
eSpecially acetoacetate, were elevated prior to meal
time.“ After feeding, total ketones rose much more rapidly
and glucose and triglyceride levels dropped faster to

pre-feeding levels in the animals fed MCT than in controls.

Clinical Applications

 

As soon as it was recognized that medium chain
triglycerides were absorbed and metabolized differently
from long chain, conventional fats, their therapeutic
usefulness became apparent. MCT is particularly helpful
in the management malabsorption disorders. In children,
where a major problem is weight maintenance and adequate

nutrition for growth when the intestinal absorptive surface

30

may be severely reduced, MCT is a good source of utilizable
kilo-calories (Gracey, et_al., 1970). In diseases of the
pancreas, especially cystic fibrosis in children, MCT has
been used to reduce the steatorrhea associated with fat
malabsbrption. MCT has also been used in the nutritional
management of children and adults with liver diseases,
although liver disorders or large portal-systemic shunts
may contraindicate use of MCT. Linscheer, et_§l. (1970)
investigated the reported narcotic effect of medium
chain fatty acids in the systemic circulation. After
administering a test dose (0.5 g per kg of lean body mass)
of MCT to cirrhotic patients and controls, it was dis-
covered that octanoate concentrations in the serum of the
cirrhotics was two times the concentration of the controls;
and the octanoate recovered in the Spinal fluid of
cirrhotics was elevated four to five times above control
values. Although no narcotic effect of the increased
octanoate to the brain was evidence in the cirrhotic
patients, reports of narcosis in research animals (Clark,
1968) may indicate caution in the use of MCT in the treat-
ment of patients with severe liver disease.

Freund and weinsier (1966) used an oral MCT
test to measure the ketone response in normal and

diabetic subjects. A standard oral dose of 25 ml of MCT

31

produced a reproducible increase in acetone concentration
ineafikexpiratory air in individual subjects, but a
dramatic difference in response was seen between controls
and diabetics. The mean ketone response of the diabetics
was 2 1/2 times greater than the response of the normal
subjects. The ketogenic prOperties of MCT have also been
used in the treatment of epilepsy in children (Medical
News, 1971). When a diet containing 60% of the total
calories as MCT was administered to a number of young
epileptics some types of seisures were reduced in number
and severity. MCT was also found to be more acceptable
to these children than the conventional 3:1 antiketogenic:

ketogenic diet.

INTRODUCTION

The 1970 ten-state nutrition survey reported
that obesity was a nutritional problem of considerable
importance in the United States. Twenty percent of white
adult males, 40% of white adult women, and 50% of black
adult women surveyed were classified as obese as
determined by skinfold thickness (Ten-State Nutrition
Survey, 1968-1970). As obesity is a risk factor in the
development of a number of serious diseases including
cardiovascular disease and diabetes mellitus (Baird,
1969), the treatment and prevention of obesity become
important health objectives.

The laboratory rat is a common model used in
studies of regulatory and metabolic obesities. Animal
studies permit rigid dietary and environmental control.
Comparisons of dietary treatments can be made in a large
number of genetically controlled situations. Changes in
body composition can be monitored accurately.

There have been indications in the literature that
increasing the content of fat in isocaloric diets may

increase growth and body fat content in growing rats

32

33

(Forbes, et_al., 1945a; 1946), increase utilization of
dietary nitrogen, and decrease the energy expense of

diet utilization for growth (Forbes, et_al., 1945b).

By feeding a diet in which 85% of the Kcal were supplied
by fat, Mickelsen, et_al. (1955) produced increased weight
gain in rats. Other investigators have shown that high
fat diets can produce increases in body fat as well as
increases in body weight in rats (Peckham, et a1, 1962;
Schemmel, et_§l., 1969; Schemmel, et al., l970a,b;
Schemmel, et al., 1972).

A number of investigators have examined body
weight gain and fat accretion in rats utilizing different
types of fat (Kaunitz, et_al,, 1958; Leveille, et_al.,
1967a; Harkins and Sarett, 1968b). Rats fed medium chain
triglycerides (MCT) tend to have lower levels of carcass
fat (Harkins and Sarett, 1968b), and lighter fat depots
(Harkins and Sarett, 1968b; Kaunitz, et_§l,, 1958). Few
investigators, however, have looked at the clinical use-
fulness of MCT in the treatment of nutitional obesity.

The purpose of the present study was to examine
the effect of substituting MCT for conventional fats on
some of the parameters of dietary obesity in rats fed

diets containing 50% (x/x) fat.

METHODS

Selection and Care of Animals

Forty-two male Osborne-Mendel rats from our
breeding colony were weaned at 21 days of age and
littermates were divided among three groups. The mean
weaning weight of the fourteen animals assigned to a group
did not differ; 55 grams for each group. The animals
were housed in metal, wire-bottomed cages in a laboratory
lighted for 12 hours of each 24 and maintained at a
temperature of 23 f 1°C. Food and water were available

ad libitum for a period of 12 weeks. Animals were weighed

 

weekly and food intakes were recorded. Food intakes were
recorded from the weight of the food cups before and

after refilling. Spillage was minimal but it was also
weighed at the time of refeeding and subtracted from intake
calculations. At 15 weeks of age the animals were

sacrificed.

Diet
Three diets (Table 1) containing 50% fat; utiliz-

ing either Crisco, corn oil, or MCT as the major source of

34

35

Kilocalories (Kcal); were fed to rats as described above.
Long chain triglycerides have a caloric value of 9.2 Kcal
per gram while Mct yields only 8.3 Kcal per gram (Kaunitz,
§E_§l., 1958). Thus the percentage of Kcal supplied

by fat was 73% for the Crisco and corn oil-containing

diets and 72% for the diet containing MCT. The diets
contained 30% protein. A calcium whey protein concentrate
was used as it was able to incorporate more oil into the
mixture. The caloriezprotein diet ratio of the MCT diet, as
calculated from Kcal consumed per gram of dietary protein
eaten, was 19.6 compared to a value of 20.3 for the Crisco
and corn oil diets. The corn oil diet was included as a
control of diet consistency, as it could be possible that
the consistency of the diet would influence its acceptibility
and consumption by the rat. Five percent Crisco was

added to each of the oil-containing diets to improve their
consistency. The rat requires 25mg. methyl linoleate per
day (Farris, 1949). Corn oil was added to the MCT diet

at the 3% level to supply this essential fatty acid.

The fatty acid composition of the 3 fats (Table 2) were

'determined by gas chromatography. The fatty acid

 

1Our laboratory is especially grateful to Dr. V. K.
Babayan for communicating his awareness of the calcium whey
protein concentrate to Dr. Olaf Mickelsen. We are grateful
to both of these men for their encouragement and continued
interest in the usefulness of MCT in human diets.

36

composition of the 3 diets (Table 3) were then calculated
from the total fat content of each diet. This explains
the presence of long chain fatty acids in the MCT diet.
A difference in color was noted among the feces produced
by rats fed the three diets. A one week fecal collection
based on weight was made for fat analysis. The feces were
dried and fat content was determined by methods similar
to tissue fat extraction. The fecal collection did not
represent individual animals nor a specific period of time
so that digestibility factors could not be determined.
Digestible Kcal per gram of diet were calculated
from the values of Merrill and Watt (1955). A value of
8.84 digestible Kcal per gram was used for Crisco and corn
oil while values of 4.27 Kcal per gram and 4.03 Kcal per
gram were used for protein and cornstarch, respectively.
Because MCT is easily hydrolyzed and absorbed, no correc-
tion was made for digestibility, and a Kcal value of
8.3 per gram of MCT was used for calculation purposes

(Kaunitz, et al., 1958).

Body Composition Analyses

 

Animals were sacrificed and prepared for body
composition analyses by the method of Schemmel, et a1.

(1969). Aliquots of carcass homogenates were analyzed for

37

moisture, fat, protein, and ash by methods closely
following those of Mickelsen and Anderson (1959).
Moisture was determined by drying the aliquots for 48
hours in a vacuum oven under high vacuum and at a
temperature of 70°C. Fat from the dried residue was
then extracted on a Goldfisch apparatus for 7 hours using
ethyl ether as the solvent. The dried, fat-free residues
were divided for protein and ash determinations. Protein
was calculated from total nitrogen as determined by the
micro-Kjeldahl method. Ashing was complete after 12
hours at 500°C.

Fat Depot Weights, Total Triglyceride

and FattyyAcid CompoSition

The left inguinal, testicular, and perirenal-
retroperitoneal fat depots were removed according to the
method of Schemmel, et_al. (l970b). Depots were
immediately wrapped in pre-weighed foil, weighed, and
stored below 0°C for further analysis.

Total triglyceride of each depot was determined
by the method of Ostrander and Dugan (1962). All
reagents were reduced by one-half and tissues were
macerated in an Omnimixerl. Measured aliquots were

removed for fatty acid analysis as well as total

 

l .
Ivan Sorvall, Inc., Newtown, Connecticut.

38

triglyceride determinations. The latter aliquot was
placed in a previously tared flask. Solvents were allowed
to evaporate overnight under a hood and flasks were dried
for one hour at 60°C before final weighing. Solvents

from aliquots for fatty acid analysis were evaporated on

a rotary evaporator in a 40°C water bath. Methylation

was by the method of Karmen, et_al. (1963). Samples were
incubated overnight at 60-65°C. The following morning 1
ml. distilled water was added to each sample and they were
stored under nitrogen below 0°C.

The methyl esters were prepared for gas chro—

matography by modifications of the method of Burchfield
and Storrs (1962) and Karmen, §t_al, (1963). Four m1.
petroleum ether and 1 ml. distilled water were added to
the methylation mixture and the petroleum ether layer
was collected. This was repeated three times after which
the petroleum ether was washed twice with 1 ml. of dis-
tilled water. The petroleum ether was evaporated using
a hot plate. Nitrogen was bubbled through the solvent
throughout the evaporation to prevent oxidation of the
unsaturated fatty acids. The methyl esters were diluted
approximately 1:5 with nanograde hexane and loaded into
a Hewlett-Packard model 402 gas chromatograph; coating,

5% DEGS; support, Chromosorb W; mesh, 80-100; carrier gas,

39

Helium; rate, 3.5 at 40psi; program, l30—200°C at 5°C/min.
Identification of peaks was by retention time of standard
mixture.l Calibration was by external normalization of
corrected peak area. Measurement of peak areas was by

height X width-at-l/Z height.

Statistical Analysis
Analysis of variance and covariance were performed
on the MSU Control Data Corporation 3600 computer using
the MSU Agricultural Experiment Station STAT series.
Scheffé confidence intervals were used in analysis of

mean values (Scheffé, 1959).

 

1Sigma Chemical Co., St. Louis, Missouri.

 

RESULTS AND DISCUSSION

Diet and Kcal Consumption

Rats fed Crisco ate a mean total of 1122 i 71
grams of diet over the 12 week feeding period; i.e.
weaning to 15 weeks of age; while rats fed corn oil or
MCT ate 1073 i 82 grams and 1014 i 80 grams, respectively,
for the same period (Table 4). Corn oil fed animals ate
5% fewer grams than the rats fed Crisco; while rats fed
the MCT diet ate 5% less grams than the rats fed corn
oil. The difference in mean values as tested by Scheffe
confidence intervals indicated that the Crisco and MCT
consumption values were significantly different (p <0.025,
Table 4a). Wiley and Leveille (1973) reported a
similar percent decrease in food intake in rats fed diets
containing 14% (w/w) corn oil or MCT when compared to
diets containing lard or coconut oil. Whether these re-
ductions in food intake were a function of food preference,
or in the case of the MCT diet, a direct effect of the
MCT on appetite because of the increase in blood

ketones (Wiley and Leveille, 1973) is not known.

40

41

The caloric density of the diets varied due to
the variation in caloric density of the constituent fats.
The Crisco and the corn oil diets contained 6.1 digestible
Kcal per gram, while the diet containing the MCT had a
calculated 5.9 digestible Kcal per gram (Table 4). When
food intakes were adjusted for the difference in
digestible Kcal per gram of diet the gap in intake
between the rats fed MCT and those fed Crisco or corn oil
widened. The average Kcal intake of the MCT-fed rats
was 5985 i 474 Kcal for the 12 weeks versus intake values
of 6842 t 433 and 6544 i 498 Kcal for rats fed Crisco or
corn oil for the same period (Table 4). The energy intake
of rats fed MCT was significantly lower over the 12 week
period (p <0.025, Table 4a).

Although no determinations of fat absorption could
be made from the fecal collection made; fat content of
the feces varied considerably. Feces from animals fed
Crisco contained 37.6 grams of fat per 100 grams of dry
fecal weight. Feces from corn oil fed animals contained
14.8% fat and fecal fat was 5.7% in rats fed MCT.

It was recognized that variation in energy intake
would tend to compound the effects of diet upon the growth
rate, if indeed, there were any effects. Ideally it would

have been beneficial to regulate food intake so that diet

42

groups consumed the same amount of Kcal during the

feeding period. One problem associated with regulation

of food intake in the rat has been that food restriction
alters the rat's normal "nibbling" pattern and produces

a "meal-eater". ‘Meal-eating in the rat has been shown

to increase food efficiency, alter gastro-intestinal tract
size, increase glucose utilization, and increase fatty
acid synthesis in adipose tissue (Leveille, 1972). In
view of these major metabolic alterations it seemed more

desirable to follow an ad libitum feeding regime and risk

 

the variation in food and caloric intakes.

Growth Rates

 

In general, growth rates for the Crisco fed, corn
oil fed, and MCT fed rats reflected the total energy
-consumed (Figure l). The mean weaning weight of all three
groups was 55 grams. Rats fed the Crisco diet attained
a final weight of 480 grams, while rats fed corn oil
reached a final weight of 454 grams. There was no
significant difference in these two rates of gain and both
groups utilized 16.6 Kcal per gram of weight gained after
weaning. Rats fed MCT weighed only 369 grams at the end
of twelve weeks and utilized 20.3 Kcal per gram of weight

gained. The MCT fed rats gained weight at a rate

43

significantly lower than either the Crisco or the corn oil
fed animals (p <0.005). Other investigators have indicated
that medium chain triglycerides may not be as efficient
in producing weight gain as longer chain triglycerides.
Harkins and Sarett (1968b) reported that rats fed a diet
containing 21% MCT (w/w) for 4 weeks utilized 8.7 Kcal
per gram of weight gained compared to 8.2 Kcal per gram
when the diet contained corn oil. These two diets produced
an 8 gram difference in mean body weight between the two
groups. After a period of weight maintenance by restrict-
ing food intake, Kaunitz, et_§l. (1958) reported a l Kcal
increase in requirement per gram of subsequent weight gain
in rats fed MCT versus those fed long chain triglycerides.
Analysis of covariance was used in an attempt to
investigate the relative significance of weaning weight,
food intake, Kcal intake, and diet on final body weight.
By statistically restricting covariates to zero it was
possible to test individual factors to indicate if they
had a significant effect upon final body weight. When
the diets were analyzed in this fashion, with the difference
in food and Kcal intake between the diets statistically
nullified, there was no significant effect of the diet on

final body weight (p <0.102). The variation in food intake

44

(p <0.012) and kcal intake (p <0.010) were much more
significant in explaining final body weight. Initial body
weight had a significant effect (p <0.001) on final body
weight, indicating that if diet and intakes are equal for
each animal, the heaviest rats at weaning will be the
heaviest rats at sacrifice. I

Simple correlation coefficients indicated signifi—
cant positive correlations between final body weight and

diet, as well as food and kcal intake (Table 10).

Body Composition

 

The greatest difference in body composition among
rats fed Crisco, corn oil or MCT was in the amount of
body fat. The mean total fat in grams of the Crisco,
corn oil, and MCT fed rats were 130.1 1 29.9, 109.2 f 21.1,
and 61.3 i 13.7 respectively (Table 5). This means MCT
fed rats had 50% less fat in their bodies than did rats
fed Crisco or corn oil. Rats fed MCT had less moisture
and protein in their bodies than did rats fed Crisco or
corn oil (Table 5). This is reflected by their lower
body weight. Only ash content showed no difference among
rats fed the different diets. Diet composition, obesity
or even severe undernutrition have little effect on body

ash if animals of the same age and sex are analyzed

45

(Schemmel, §t_al., 1969; Pratt and McCance, 1960).
Because the MCT fed rats were also lower in total carcass
weight, the body composition values were expressed as
grams per 100 grams of body weight (Table 6). The car-
casses of the Crisco and corn oil fed rats contained a
mean value of 26.9 t 4.5 and 23.9 r 2.9 grams of fat per
100 grams of body weight. The MCT—fed rats averaged
only 16 r 2.8 grams of every 100 grams of body weight as
fat..

Energy utilization was calculated from Kcal con-
Sumed per gram of fat gained after weaning. Body com-
position of male warding Osborne-Mendel rats as reported
by Schemmel, §t_al. (1969) were subtracted from total
body fat of the animals in the present study. Animals
receiving Crisco or corn oil diets utilized, respectively,
54 and 62 Kcal per gram of fat gained after weaning; while
MCT fed rats utilized 105 Kcal per gram of body fat gained.
In a study of the effects of diet and strain in the
production of obesity in rats, Schemmel, gt_al. (1970a)
reported that, although ration and strain influenced weight
gain equally, the composition of the ration seemed to have
more influence on body fat accretion.

Again, the variation in food and Kcal intake

could have affected body composition, but it was possible

46

to account for this statistically. The analysis of
covariance routine used allowed for the restriction of
designated covariates to zero. Thus it was possible to
analyze the covariance of diet and body composition
without the effects of food intake, or the covariance of
food and energy intakes with body composition ignoring

the difference in diet. In this manner it was statisti-
cally possible to examine individual factors which could
not be separated in the experimental design. Diet, food
intake and kcal intake had no statistically significant
effect on body composition when these factors were examined
Iindividually. Initial body weight was a significant
influence on moisture (p <0.078), fat (p <0.053), and
protein (p <0.098), but not on ash, when all other factors

were excluded. The fact that diet and intake had no

statistical significance in determining body composition

could merely indicate that diet differences or intake

variations alone could not account for changes in body
composition; but combinations of these factors may be
important.

Percent moisture and protein showed high negative

correlations with final body weight while percent body fat

had a high positive correlation (Table 11). The same is

true when food and kcal intakes were examined.

47

The relative amount of protein showed negative correlations
to food and Kcal intake. It is interesting to note the
high negative correlation of percent body moisture to per-
cent body fat (-0.989) which indicates why body moisture

is often used to estimate lean body mass.

Fat Depot Weights

 

Fat depot weights also varied among the three diet
groups. The mean inguinal fat depot weight in the MCT
fed rats weighed 7.8 i 2.4 grams while the same depot
weighed an average of 15.7 r 5.3 grams and 12.3 i 3.4 grams
in the Crisco and corn oil-fed animals, respectively
(Table 7). The decrease in the inguinal depot weight of
the MCT-fed animals was only significant when compared to
the depot weight of the Crisco—fed rats (Table 7a). A
high standard deviation was seen in the inguinal fat
depot weight in individual animals. The standard
deviation of the depot weight for rats fed Crisco diets
was 33% of the mean value (Table 7). It does not seem
possible that this variability was caused by the dissection
technique. Schemmel, §t_al. (l970b) reported only minimal
differences in right and left depot weights removed by the
technique used in the present study. The inguinal fat

depot also was the heaviest fat depot of the 3 weighed in

48

rats of all three diet groups. Shier and Schemmel (in
press) reported that inguinal fat depots tended to be
greater in weight than the testicular or perirenal-
retroperitoneal depots until the rats reached approximately
20 weeks of age; at which time the perirenal-retro-
peritoneal depot weight approached that of the inguinal
depot and surpassed the weight of the inguinal depot in
older rats (Schemmel, gt_al., 1970b). The amount of
subcutaneous fat seemed to be more variable than the
amount of intraabdominal fat. The testicular and
perirenal-retroperitoneal fat depots gained less weight in
rats fed MCT than in rats fed corn oil or Crisco diets.
This is likely to be associated with the fact that
development of these depots is delayed. Mean weight of
the testicular fat depots of MCT fed rats was 2.4 i 0.4

grams; which was significantly lower (p <0.025) when com-l

rats which averaged 8.0 i 2.6 and 5.4 i 1.6 grams in

weight, respectively. The average weights of the perirenal-
retroperitoneal depots were MCT, 3.2 r 1.1 grams; Crisco,
9.2 r 2.2 grams; and corn oil, 7.0 i 2.2 grams, respec-
tively. Mean weight of the perirenal-retroperitoneal

depots was also significantly lower in the MCT fed animals

49

(p <0.025) when compared to Crisco or cornuoil fed rats.
Even when depot weights were expressed as grams per 100
grams of body weight there was a 33% decrease in the
relative weight of the inguinal depot of the MCT-fed

rats when compared to the same depot of the Crisco—fed
rats (Table 7). The relative weights of the other two
depots decreased by over 50% when the values, as percent
of body weight, were compared for these two groups.
Kaunitz, et_al. (1958) had reported that testicular fat
depots weighed 0.84 grams per 100 grams of body weight in
male Sherman rats fed MCT compared to values of 1.05

grams per 100 grams of body weight for rats fed long chain
triglycerides. Harkins and Sarett, (1968b) reported a

2 gram difference between the weights of the epididymal
fat depot in MCT and corn oil—fed animals which represented
a decrease of 0.3 grams per 100 grams of body weight in
the depot of the MCT-fed animals.

Fat depot weights were the only parameters
analyzed by restricted covariance in which the diet alone
significantly affected the variation in depot weights
(inguinal, p <0.067; testicular, p <0.083; perirenal—
retroperitoneal, p <0.079). Initial body weight had no

effect on fat depot weights when all other factors were

50

zero. Variation in food and Kcal intakes had no effect
on testicular depot weights, while the inguinal and
perirenal-retroperitoneal depot weights were affected
significantly (p <0.03; p <0.08). All three fat depots
showed high positive correlations to final body weight

as well as to food and Kcal intake (Table 12).

Fat Depot Triglyceride Content

 

There was no significant difference in the trigly-
ceride content of the inguinal, testicular, and perirenal—
retroperitoneal fat depots of rats fed Crisco, corn oil,
or MCT when similar depots were compared among the three
groups (Table 8, 8a).‘ There did seem to be a tendency for
-the intraabdominal depots to contain more fat per 100
grams of tissue (Table 8). Shier and Schemmel (in press)
reported less triglyceride per gram of tissue in inguinal
depots when compared to testicular or perirenal-retro—
peritoneal depots, as well as an increase in total tri-
glyceride content of the intraabdominal fat depots with age
until values over 90% were reached. Subcutaneous depots

never reached triglyceride levels of 90% of tissue weight.

51

Fat Depot Fatty Acid Composition

 

Borgstrom (1955) found that medium chain fatty
acids were rapidly cleared by the liver and a concentration
of 4.7 mg% decanoic acid in the portal blood was reduced
to 1.5 mg% in vena cava blood. Leveille, gt_§1. (1967a)
found little medium chain fatty acids in the peripheral
circulation of rats fed MCT. The review of literature
pointed out that other investigators have found little
incorporation of MCT into adipose tissue lipids (Leveille,
§t_gl., 1967a; Harkins and Sarett, 1968b; Kaunitz and
Johnson, 1968; Tamir, gp_al., 1969). The present study
confirmed this fact. Even though 53% of the dietary Kcal
were supplied by C8 and C10 fatty acids, and these fatty
acids were fed during the period of greatest body growth,
only a small increase occurred in these components of
adipose tissue (Table 9). It seems as if the relative
increase in incorporation of medium chain fatty acids is
not easily altered by increasing the dietary level of
these fatty acids. In this study where the dietary intake
of MCT was very high, as well as in other studies where
MCT made up a relatively lower prOportion of dietary Kcal
(Leveille, ep_al., 1967a; Harkins and Sarett, 1968b;
Kaunitz and Johnson, 1968), there has been a shift toward

similar increases of MCT in the fat pads of rodents.

SUGGESTION FOR FURTHER STUDY

Plasma Free Fatty Acids and Triglycerides

 

One of the important properties of medium chain
fatty acids is their rapid and almost complete oxidation
by the liver. When the liver's ability to oxidize MCFA
is impaired narcosis may be produced by increased plasma
free fatty acids entering the spinal fluid and the brain
(Linscheer, gp_al., 1970). Further study on the metabolism
of MCT should include post absorption determination of the
capacity of the normal liver to clear these free fatty

acids from the blood during MCT administration.

Food Preference

 

The Kcal intake of the MCT diet was considerably
lower than either of the other two diets. Whether this
decrease was due to a decreased rat preference for the MCT
diet, or a direct effect of the MCT diet on appetite

should be investiaged further.

Fat Digestibility

 

Determinations of fat digestibility were not con-

ducted during the present study. The fecal fat content of

52

 

. 1 IE I- ..III ‘1' E 1 El E1 till“ i w

53

the rats fed Crisco, Corn oil and MCT diets varied widely.
Further study should be done to examine the digestibility
of these 3 fats at the high level used in the present

study.

Fat Soluble Vitamin Absorption

 

Relatively little is known of the normal vehicle
for the absorption of fat soluble vitamins. The question
was raised as to the changes in absorption of nutrients
that require fat as an absorption vehicle that might occur
during MCT absorption. If medium chain triglyceride
absorption differs from normal fat absorption, are the
fat-soluble vitamins affected by this change? Kaunitz,
gp_§l. (1968) reported less severe testicular damage in
vitamin E deficient rats fed MCT when they were compared
to deficient rats without MCT in the diet. While investi-
gations are being conducted into the mechanisms of fat-
soluble vitamin absorption it must be remembered that all

fats are not absorbed in like manner.

Effects on Human Obesity

 

Animal studies can only give an indication of what
may be applied to human situations. The decreased caloric

efficiency of MCT and its influence in producing smaller

 

54

body weight gains and decreased body fat accretion should
be investigated in human subjects.

Clinical use of MCT oils is already widespread as
indicated in the literature review. Food products have
been developed incorporating MCT oil in place of con-
ventional fats (Schizas, gt_§1,, 1967). A clinical study
of the effect of the substitution to MCT in human diets
would help to establish the effectiveness of MCT as an

aid in the treatment of obesity.

 

Jill I .
l l Ii] l Ell. .illl'p Ii

CONCLUSIONS

The decreased caloric value of medium chain
triglycerides (MCT) decreased the caloric density of the
diet containing this fat. Combined with the fact that
food intake was lower in the rats fed the MCT diet, their
total Kcal intake was significantly lower than the animals
fed Crisco or corn oil-containing diets.

Growth rates were similar for the Crisco and corn
oil-fed rats over the 12 week feeding period. Rats fed
MCT grew slower and reached an average final body weight
of 369:20 grams, which was significantly lower than final
body weights of animals fed either Crisco or corn oil.
Crisco fed animals attained final weights of 480:49 grams
while rats fed corn oil weighed 454:36 grams at the end
of 12 weeks.

Body composition analyses showed that absolute
and relative body fat were decreased in animals fed MCT-
diets. The absolute and relative weights of the inguinal
testicular and perirenal fat depots were also lower in MCT

fed animals while no significant differences were found in

55

56

triglyceride content of the depots among animals of the
three diets. Inguinal fat depot fatty acid composition
showed a slight increase in C8 and C10 fatty acids. A
The diet containing 50% MCT did not contribute to
the obesity normally found in rats fed a high fat diet.
Animals fed MCT contained only 16.5r2.8 grams of fat per
100 grams of body weight, while Crisco-fed rats had
26.9:4.5 grams of fat for every 100 grams body weight and
corn oil-fed rats contained 23.9:2.9 grams of fat per
100 grams body weight. It seems that much of this effect
could be attributed to the decreased caloric intake of
the rats fed the MCT diet. There was, however, a
difference in the utilization of dietary Kcal for weight
gain among the three diets examined. Rats fed the MCT
diet utilized 20.3 Kcal per gram of weight gained while
Crisco and cornboil fed animals utilized 16.6 Kcal per
gram of weight gain. This data indicates that MCT may _
be beneficial in increasing the expense of energy
utilization of high fat diets and preventing some of the

body weight gain and increase in body fat found in animals

raised on such diets.

57

 

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58

TABLE 2.--Fatty acid composition of Crisco, corn oil,
and MCT. (Values are expressed as percentage

of the total fatty acids in the fat)

 

 

 

Fatsa

Fatty Acids Crisco Corn Oil MCT
8:0 - - 72.0
10:0 - - 28.0
12:0 - - -
14:0 - - -
16:0 18.2 9.9 -
16:1 - - -
18:0 12.4 1.6 -
18:1 41.5 21.2 -
18:2 27.5 66.2 -
18:3 trace trace -
20:0 — trace -
20:4 - - -

 

aMean value of samples done

in duplicate.

59

TABLE 3.--Fatty acid composition of Crisco, corn oil,
and MCT diets. (Values are eXpressed as
percentage of the total fatty acids in each

 

 

 

diet)
Dieta

Fatty Acids Crisco Corn Oil MCT
8:0 - - 60.5
10:0 - - 23.5
12:0 - - -
14:0 - - -
16:0 18.2 10.9 2.4
16:1 - - -
18:0 12.4 2.6 1.3
18 1 41.5 23.2 5.4
18 2 27.5 ‘62.4 6.7
18.3 trace trace -
20.0 - trace -
20:4 - - -

 

aValues calculated from fatty acid composition of
the fat and total fat composition of the diet.

60

TABLE 4.--Dietary intake of male Osborne - Mendel rats fed
high fat diets containing Crisco, corn oil, or MCT
for 12 weeks; and conversion factors for determining
energy and Kcal:protein ratio in the rations.

 

 

Diet Kcal/g.dieta Kcal:Proteinb Diet Intake
9. Kcal.
Crisco (14)C 6.1 20.3 11223271d 6842:433
Corn Oil (14) 6.1 20.3 1073182 6544:498
MCT (13) 5.9 19.6 1014180 5985:474

 

aSee text for explanation of calculations.
bKcal consumed per gram of protein consumed
cNumber of rats
dMean 1 standard deviation

TABLE 4a.--Scheffe confidence intervals (0.975) for all

possible contrasts of mean differences in total
diet consumption and total Kcalorie consumption.

 

Scheffe Confidence Intervals

 

Diet Intake Dietary Intake

 

Diets g Kcal.
Crisco vs. Corn oil 48:84: 297:512*
Crisco vs. MCT 107:86 856:522*
Corn oil vs. MCT 58:86 559:522

 

 

ail - fiztS/Mse(1/n+l/n)

*Significant at p <0.025

 

Body Weight (g)

61

500 "
.g.
- ____. Crisco (l4)* /O-.
....._.. Corn Oil (14) /
400 ‘—' ---- MCT (13) /

 

 

 

300
200
100
J
+ 3 6 9 12
Weaning Weeks of Feeding

Figure l.--Mean growth rates of male Osborne-Mendel
rats fed high fat diets containing Crisco, corn oil or MCT
for 12 weeks from the time of weaning at 21 days of age.

 

*
Number of animals.

62

TABLE 5---Absolute body composition of Osborne—Mendel male
rats fed high fat diets containing Crisco, corn
oil, or MCT for 12 weeks.

 

Body Composition

 

 

Diet Carcassa Moisture Fat Protein Ash
9. g. g. g. g.
Crisco (6)b 480.41.49.1C 253.0:222 l30.l:':29.9 83.515. 6 ll. 0i0.3
Corn Oil (6) 454.5i36.3 245.3il3.4 1092121.]. 84515.0 11. 510.5
MCT (6) 369.6120.4 221.21 4.1 61.311337 74312.4 11.1i0.6

 

aCarcass wt. = live weight - weight of G.I. contents
bNumber of rats in diet group

cMean 1 standard deviation

TABLE 5a.--Scheffe confidence intervals (0.975) for all pos-
sible contrasts of mean differences in body

 

 

 

composition.
Scheffe Confidence Intervals
Diet Carcass Moisture Fat Protein Ash
Crisco vs. Corn oil 25. 9+65. 4a 7. 7+26. 7* 20. 9+39. 6* 1. 0:8. 0* 0.5:0.8
Crisco vs. NEH? 110. 8- 65. 4: 31. 8+26. 7* 68. 7+39. 6* 8. 618. 0* 0.110.8
Corn.oil vs. MCT 84. 9165. 4 24.1126. 7 47. 9+39. 6* 9. 6:8. 0 0.410.8

 

 

ail £112 3 /Mse (1/n+1/n)

*Significant at p <0.025

 

63

TABLE 6.--Relative body composition of Osborne-Mendel male
rats fed high fat diets containing Crisco, corn

oil, or MCT for 12 weeks.

 

gBody Composition_.

 

Moisture Fat

 

Diet Protein Ash
g/lOOg ma g/lOOg 13w g/lOOg dry FFIb g/lOOg dry m .
Crisco (6)° 52.9i3.4d 26.914.S 35.9iz.o 11.4i0.8
Corn oil (6) 54.1t2.3 23.9iz.9 84. _ . 11.5io.3
MCT (6) 60.012.3 16.5i2.3 86.1tl.7 12.810.6

 

aGrams per 100 grams of body weight

bGrams per 100 grams of dry, fat-free tissue

cNumber of rats in each diet group

dMean i standard deviation.

TABLE 6a.--Scheffe confidence intervals (0. 975) for all
possible contrasts of mean differences in body

composition.

 

Diets

Scheffe Confidence Intervals

 

Moisture Fat

Protein Ash

 

Crisco vs. Corn oil 1.214. 8a 3. 0+6. 1*
Crisco vs. MCT 7.1+4. 8: 10. 4+6. 1:
Corn oil vs. MCT 5. 914. 8 7. 416. 1*

.1 0.111.1*

.213.1 1. 411.1:
.613.1 1. 311.1

 

 

ail e 32 s/ffise<1/n+1/n)
*Significant at p <0.025

64

TABLE 7. n-Relative inguinal, testicular, and perirenal-
retroperitoneal fat depot weights of Osborne-
Mendel male rats fed high fat diets contain-'
ing Crisco, corn oil, or MCT for 12 weeks.

 

 

 

Fat Depots
Perirenal-
Inguinal Testicular RetrOperitoneal
Diet ga g/lOOg BWb g g/lOOg BW g g/lOOg BW
Crisco (8) d 15. 75. 3c 3.3 8. 012.6 1.7 9.2iz.2 1.9
Corn oil (8) 12. 313. 4 2.7 5. 411. 6 1.2 7.012.2 1.5
MCT (7) 7. 812. 4 2.2 2. 410.4 0.6 3.2.41.1 0.9

 

 

a Grams
bGrams per 100 grams of body weight
cMean 1 standard deviation

dNumber of rats

TABLE 7a.--Scheffe confidence intervals (0.975) for all pos-
sible contrasts of mean differences in fat depot
weights (grams).

 

Scheffe Confidence Intervals

 

 

 

 

Perirenal—
Diets Compared Inguinal Testicular Retroperitoneal
Crisco vs. Corn oil 3.4is.9i 2.612.7* 2.312.9*
Crisco vs. MCT 7.916.l 5.612.8* 6.013.0*
Corn 011 vs. MCT 4.516.1 3.112.8 3.813.0
a-

“1 - 172 i sfmseu/ml/n)

*Significant at p <0.025

65

TABLE 8.--Re1ative weight of triglyceride in inguinal,
testicular, and perirenal-retroPeritoneal fat
depots of male Osborne-Mendel rats fed high fat
diets containing Crisco, corn oil, or MCT for

 

 

 

12 weeks.
Fat Depot
Perirenal-

Inguinal Testicular Retroperitoneal

g/IOOga .g/1009 9/1009
Crisco <8)b 78.6rs.4c 88.7i3.o 88.613.2
Corn Oil (8) 75.2:3.0 89.614.3 87.313.2
MCT (7) 72.513.0 83.615.4 84.713.4

 

aGrams per 100 grams of depot weight

bNumber of rats

CMean 1 standard deviation

TABLE 8a.--Scheffe confidence intervals (0.975) for all
possible contrasts of mean differences of
relative weight of triglyceride in fat depots.

 

Scheffe Confidence Intervals

 

 

Perirenal-
Diets Inguinal Testicular Retroperitoneal
Crisco vs. Corn oil 3.416.3a 0.9r6.6 1.3r4.8
Crisco vs. MCT 6.1:6.3 5.1:6.9 3.9iS.O
Corn oil vs. MCT 2.716.5 6.017.0 2.615.0

 

 

ail - 52 i s/rmse(1/n+1/n)w

66

TABLE 9.--Mean fatty acid composition of inguinal fat depot
of male Osborne-Mendel rats fed high fat diets
containing Crisco, corn oil, or MCT. (Values are
expressed as percent of total fatty acids.)

 

 

 

Diet
Fatty Acid Crisco (8)a .Corn oil (8) MCT (7)
8:0 - - <1
10:0 - - 2.0
12:0 trace trace <1
14:0 <1 <1 <1
16:0 3.7 3.5 6.7
16:1 2.0 1.1 3.7
18:0 6.7 3.1 7.2
18:1 53.1 34.7 46.1
18:2 33.7 57.2 32.4
18:3 <1 <1 <1
20:0 trace trace trace
20:4 trace trace trace

 

aNumber of depots

 

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BIBLIOGRAPHY

Allee, G. L., D. R. Romsos, G. A. Leveille and D. H. Baker.
1972. Metabolic consequences of dietary medium-chain
triglycerides in the pig. P.S.E.B.M. 139: 422-427.

Alonso, Lillian G. and Thomas H. Maren. 1955. Effect of
food restriction on body composition of hereditary
obese mice. Am. J. Physiol. 183: 284-290.

Babayan, V. K. 1968. Medium-chain triglycerides - their
composition, preparation, and application. J.A.O.C.S.
45: 23—25.

Baird, I. McLean. 1969. Obesity in adults. In: Obesity,
Medical and Scientific Aspects. I. McLean Baird and
Alan N. Howard, eds. London: E. & S. Livingstone Ltd.

Behnke, Albert R. 1952. The relation of lean body weight
to metabolism and some consequent systematizations.
Ann. N.Y. Acad. Sci. 56: 1095-1142.

Behnke, Albert R. 1964. Role of fat in gross body come
position and configuration. In: Fat as a Tissue.
K. Rodahl and B. Issekutz, eds. New York: McGraw-Hill
Co.

 

Bloom, B., I. L. Chaikoff and W. O. Reihardt. 1951.
Intestinal lymph as pathway for transport of absorbed
fatty acids of different chain lengths. Amer. J.
Physiol. 166: 451-455.

Borgstrom, Bengt. 1955. Transport form of 14C-decanoic
acid in porta and inferior vena cava blood during
absorption in the rat. Acta Physiol. Scand. 34:
71-74.

Bray, G. A. 1970. Metabolic and regulatory obesity in rats
and man. In: Adipose Tissue, Regulation and
Metabolic Functions. B. Jeanrenaud and D. Heppr eds.
New York: Academic Press.

 

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BIBLIOGRAPHY

 

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Brobeck, John R. 1946. Mechanism of the development of
obesity in animals with hypothalamic lesions.
Physiol. Rev. 26: 541-559.

Brobeck, John R. 1955. Neural regulation of food intake.
Ann. N.Y. Acad. Sci. 63: 44-55.

Bruch, Hilde. 1955. Role of emotions in hunger and
appetite. Ann. N.Y. Acad. Sci. 63: 68-75.

Burchfield H. P. and Eleanor E. Storrs. 1962. Bio-
chemical Applications of Gas Chromatography. New
York: Academic Press.

Clark, Suzanne Bennet. 1968. Limiting factors in
maximal steady state absorption of medium chain
triglycerides. In: Medium Chain Triglycerides.
John R. Senior, ed. Philadelphia: University of
Pennsylvania Press.

 

Clark, Suzanne Bennet and Peter R. Holt. 1969. Inhibition
of steady-state absorption of long-chain triglyceride
by medium-chain triglyceride in the unanesthetized
rat. J. Clin. Invest. 48: 2235-43.

Desnuelle, P. and P. Lavary. 1963. Specificities of
lipases. J. Lipid Res. 4: 369-384.

Devi, J. P. Saroj, F. Zavier Pi-Sunyer and Sami A. Hashim.
1969. Effect of odd and even numbered medium chain
fatty acids on glucose uptake by adipose tissue.
P.S.E.B.M. 132: 632-635.

Duncan, Garfield G., Theodore G. Duncan, Guy Lacy Schless
and Fred C. Cristonfoni. 1965. Contraindications
and therapeutic results of fasting in obese patients.
Ann. N.Y. Acad. Sci. 131: 632-636.

Fenton, Paul F. and Marian T. Dowling. 1953. Studies on
obesity. I. Nutritional obesity in mice. J. Nutr.
49: 319-331.

Forbes, E. B., R.W. Swift, R. F. Elliott and W. H. James.
1945a. Relation of fat to economy of food

utilization. I. By the growing albino rat. J. Nutr.
31: 203-2/2.

Forbes, E. B., R. W. Swift, R. F. Elliott and W. H. James.
1945b. Relation of fat to economy of food
utilization. II. By the mature albino rat. J. Nutr.
31: 2/3-227.

 

71

Forbes, E. B., R. W. Swift, W. H. James, J. W. Bratzler and
Alex Black. 1946. Further experiments on the relation
of fat to economy of food utilization. I. By the
growing albino rat. J. Nutr. 32: 387—403.

Freund, Gerhard and Roland L. Weinsier. 1966. Standardized
ketosis in man following medium chain triglyceride
ingestion. Metabolism. 15: 980-991.

Gracey, Michael, Valerie Burke and Charlotte M. Anderson.
1970. Medium chain triglycerides in paediatric
practice. Arch. Dis. Child. 45: 445-452.

Greenberger, Norton J., John B. Rodgers and Kurt J.
Isselbacher. 1966. Absorption of medium and long
chain triglycerides: Factors influencing their
hydroloysis and transport. J. Clin. Invest. 45:
217-227.

Hagerman, Larry M., Robert W. Harkins and Herbert P. Sarett.
1969. Hydrolysis and absorption of mediumrchain
triglycerides and soy oil. P.S.E.B.M. 131: 1028-
1033.

Hamburger, Walter W. 1957. Psychological aspects of
obesity. Bull. N.Y. Acad. Med. 33: 771-782.

Hashim, Sami A., Stanley S. Bergen, Jr., Kenneth Krell and
Theodore B. Van Itallie. 1964. Intestinal absorption
and mode of transport in portal vein of medium chain
fatty acids. J. Clin. Invest. 43: 1238.

Hashim, Sami A. and Theodore B. Van Itallie. 1965.
Studies in normal and obese subjects with a
monitored food dispensing device. Ann. N.Y.
Acad. Sci. 131: 654-661. .

Hashim, Sami, A. 1967. Medium-chain triglycerides Clinical
and metabolic aspects. J.A.D.A. 51(3): 221-227.

Harkins, Robert W., John B. Longnecker and Herbert P.
Sarett. 1964. The effect of the type and level of
dietary fat on gastric retention in rats.
Gastroenterology. 47: 65-71.

Harkins, Robert W. and Herbert P. Sarett. 1968a. Medium-
chain triglycerides. J.A.M.A. 203(4): 272-274.

Harkins, Robert W. and Herbert P. Sarett. 1968b.
Nutritional evaluation of_medium-chain triglycerides
in the rat. J.A.O.C.S. 45: 26-30.

72

Hellman, Bo. 1965. 'Studies in obese-hyperglycemic mice.
Ann. N.Y. Acad. Sci. 131: 541-558.

Hoffman, Alan F. 1968. Intraluminal factors in the
absorption of glycerides. In: Medium Chain
Triglycerides. John R. Senior, ed. Philadelphia:
University of Pennslyvania Press.

 

 

Holt, Peter R. 1967. Medium chain triglycerides: A use—
ful adjunct in nutritional therapy. Gastroenterology.
56: 961-966.

Isselbacher, Kurt J. 1968. Mechanisms of absorption of
medium chain triglycerides. In: Medium Chain
Triglycerides. John R. Senior, ed. Philadelphia:
UniVersity of Pennslyvania Press.

 

 

Janowitz, Henry D. and Franklin Hollander. 1955. The time
factor in the adjustment of food intake to varied
caloric requirement in the dog: A study of the
precision of appetite regluation. Ann. N.Y. Acad.
Sci. 63: 56-67.

Jordan, Henry. 1973. In defense of body weight. J.A.D.A.
62: 17-21.

Karmen, Arthur, Malcolm Whyte and DeWitt S. Goodman. 1963.
Fatty acid esterification and chylomicron formation
during fat absorption. 1. Triglycerides and choles-
terol esters. J. Lipid Res. 4: 312-321.

Kaunitz, Hans, Charles A. Slanetz, Ruth Ellen Johnson, Vigen
K. Babayan and George Barsky. 1958. Relation of
saturated, medium and long-chain triglycerides to
growth, appetite, thirst and weight maintenance
requirements. J. Nutr. 64: 513-524.

Kaunitz, Hans and Ruth Ellen Johnson. 1968. Nutritional
properties of medium-chain triglycerides. J.A.O.C.S.
45: 19-22.

Kekwick, A. and G. L. S. Pawan. 1956. Caloric intake in
relation to body-weight changes in the obese. Lancet.
271: 155-161.

Kennedy, G. C. 1950. The hypothalamic control of food intake
in rats. Proc. Roy. Soc. Sci. B. 137: 535-549.

 

73

Kennedy, G. C. 1953. The role of depot fat in the
hypothalamic control of food intake in the rat. Proc.
Roy. Soc. London. 149: 578-592.

King, James R. and Donald S. Farner. 1965. Studies of fat
deposition in migratory birds. Ann. N.Y. Acad. Sci.
131: 422-440.

Kleiber, Max and H. H. Cole. 1950. Body size, growth rate,
and metabolic rate in two inbred strains of rats. Am.
J. Physiol. 161: 294-299.

Lebon, P. 1969. Introduction. In: Obesity, Medical and
Scientific Aspects. I. McLean Baird and Alan N.
Howard, eds. London: E. & S. Livingstone Ltd.

 

 

Lee, Daisy, 3., Sami A. Hashim and Theodore B. Van Itallie.
1968. Effect of long chain triglyceride on chylous
transport of medium chain fatty acids. Amer. J.
Physiol. 214: 294-297.

Leveille, Gilbert A., Roland S. Pardini and Jerry Ann
Tillotson. 1967a. Influence of medium-chain

triglycerides on lipid metabolism in the rat. Lipids.
2: 287-294.

Leveille, Gilbert A., Roland S. Pardini and Jerry Ann
Tillotson. 1967b. Influence of medium-chain
triglycerides on lipid metabolism in the chick.
Lipids. 2: 461-466.

Leveille, Gilbert A. 1972. Lypogenic adaptations related
to pattern of food intake. Nutr. Rev. 30: 151-155.

Liebelt, Robert A., S. Ichinoe and N. Nicholson. 1965.
Regulatory influences of adipose tissue on food intake
and body weight. Ann. N.Y. Acad. Sci. 131: 559-582.

Lieber, Charles 8., Andre Lefevre, Norton Spritz, Lawrence
Feinman and Leonore M. DeCarli. 1967. Difference in
hepatic metabolism of long-and medium-chain fatty
acids: The role of fatty acid chain length in the
production of the alcoholic fatty liver. J. Clin.
Invest. 46: 1451-1460.

 

74

Lincheer, William G" Andre L. Blum and R. Ryan Platt. 1970.
Transfer of medium chain fatty acids from blood to
Spinal fluid in patients with cirrhosis. Gas-
troenterology. 58: 509-515.

Lloyd, June K. 1969. Obesity in childhood. In: Obesity,
Medical and Scientific Aspects. I. McLean Baird and
Alan N. Howard, eds. London; E. & S. Livingstone Ltd.

Mayer, Jean. 1957. Correlation between metabolism and
feeding behavior and multiple etiology of obesity.
Bull. N.Y. Acad. Med. 33: 744-782.

Mayer, Jean. 1965a. Genetic factors in human obesity.
Ann. N.Y. Acad. Sci. 131: 412-421.

Mayer, Jean. 1965b. Inactivity as a major factor in
adolescent obesity. Ann. N.Y. Acad. Sci. 131:
502-506.

Medical News. 1971. Special diet containing MCT benefits
epileptics. J.A.M.A. 217(9): 1179-1180.

Medium Chain Triglycerides. 1968. John R. Senior, ed.
Philadelphia: University of Pennsylvania Press.

 

Merrill, A. L. and B. K. Watt. 1955. Energy Value of Foods,
Basis and Derivation, Agricultural Handbook No. 74.
Washington, D.C.: Agricultural Research Service,
U.S.D.A.

 

 

Mickelsen, Olaf, Samual Takahashi and Carl Craig. 1955.
.Experimental obesity. I. Production of obesity in
rats by feeding high-fat diets. J. Nutr. 57: 541-553.

Mickelsen, Olaf and Arnett A. Anderson, 1959. A method
for preparing intact animals for carcass ana1y51s.
J. Lab. and Clin. Med. 53: 282-290.

Miller, Neal E. 1955. Short comings of food consumption as
a measure of hunger; results from other behavioral
techniques. Ann. N.Y. Acad. Sci. 63: 141-143.

Monello, Leonore F., Carl C. Seltzer and Jean Mayer. 1965.
Hunger and satiety sensations in men, women, boys
and girls: a preliminary report. Ann. N.Y. Acad.
Sci. 131: 593~602.

Ostrander, Joyce and L. R. Dugan, Jr. 1962. Some differences
in composition of covering fat, intermuscular fat, and
intramuscular fat of meat animals. J.A.O.C.S. 39:
178-181.

 

75

Palmer, Leroy S., Cornelia Kennedy, Charles E. Calverley,
Cecil Lohn and Paul H. weswig. 1946. Genetic
differences in the biochemistry and physiology
influencing food utilization for growth in rats.
University of Minnesota: Agricultural Experiment
Station Technical Bulletin No. 176.

Peckham, S. C., C. Entenman and H. W. Carroll. 1962. The
influence of a hypercaloric diet on gross body and

adipose tissue composition in the rat. J. Nutr. 77:
187-197.

Pike, Ruth L. and Myrtle L. Brown. 1967. Nutrition: An
Integrated Approach. New York: John Wiley & Sons, Inc.

Playoust, Marc R. and Kurt J. Isselbacher. 1964. Studies
on the intestinal absorption and intramucosal lipolysis
of a medium chain triglyceride. J. Clin. Invest. 43:
878-885.

Pratt, C. W. M. and R. A. McCance. 1960. Severe under—
nutrition in growing and adult animals. 2. Changes
in the long bones of growing cockerels held at fixed
weights by undernutrition. Brit. J. Nutr. 14: 75-84.

The Rat in Laboratory Investigation. 1949. Edmond J.
Farris and John Q. Griffith, Jr., eds. Philadelphia:
J. B. Lippincot Company.

Scheffe, Henry. 1959. The Analysis of Variance. New York:
John Wiley & Sons, Inc.

 

Scheig, Robert and Geiild Klatskin. 19684 Hepatic
metabolism of l- C ostanoic and l- C palmitic acids.
J.A.O.C.S. 45: 31-33.

Schemmel, Rachel, Olaf Mickelsen and Zeki Tolgay. 1969.
Dietary obesity in rats: influence of diet, weight,

age, and sex on body composition. Amer. J. Physiol.
216: 373-379.

Schemmel, Rachel, Olaf Mickelsen and J. L. Gill. 1970a.
Dietary obesity in rats: body weight and body fat
accretion in seven strains of rats. J. Nutr. 100:
1041-1048.

76

Schemmel, Rachel, Olaf Mickelsen and Ulrey'Mostosky. l970b.
Influence of body weight, age, diet and sex on fat
depots in rats. Anat. Rec. 166: 437-446.

Schemmel, Rachel, Olaf Mickelsen and Kamal Mbtawi.‘ 1972.
Conversion of dietary to body energy in rats as

affected by strain, sex and ration. J. Nutr. 102:
1187-1198.

Senior, John R. 1964. Intestinal absorption of fats. J.
Lipid Res. 5: 495-521.

Sherman, Charles D., Jr., Allyn G. May, William Nye and
Christine Waterhouse. 1965. Clinical and metabolic
studies following bowel by-passing for obesity. Ann. -
N.Y. Acad. Sci. 131: 614-622. 1

 

Shier, Patricia D. and R. Schemmel. In Press. Dietary
strain, and age effects on composition and growth of
fat depots in male rats. P.S.E.B.M.

Stauffacher, Werner, Oscar B. Crofford, Bernard Jeanrenaud
and Albert E. Renold. 1965. Comparative studies of
muscle and adipose tissue metabolism in lean and obese
mice. Ann. N.Y. Acad. Sci. 131: 528-540. '

Steinbock, H., Margaret House Irwin and Janet Weber. 1936.
The comparative rate of absorption of different fats.
J. Nutr. 12: 103-111.

Stickney, Robert R. and James W.Andrews. 1972. Effects
of dietary lipids on growth, food conversion, lipid and
fatty acid composition of channel catfish. 'J. Nutr.
102: 249-258.

Stunkard, Albert J. 1955. Untoward reactions to weight
reduction among certain obese persons. Ann. N.Y.
Acad. Sci. 63: 4-5.

Stunkard, Albert J. 1957. The "dietary depression."
Incidence and clinical characteristics of untoward

responses to weight reduction regimens. Am. J. Med.
23: 77-86.

Stunkard, Albert. 1959. Obesity and the denial of hunger.
Psychosom. Med. 21: 281-289.

77

Stunkard, Albert and Myer Mendelson. 1967. Obesity and
the body image: I. Characteristics of disturbances in
the body image of some obese persons. Amer. J.
Psychiat. 123: 1296-1300.

Swift, Raymond W. and Cyrus E. French. 1954. Energy
Metabolism and Nutrition. Washington, D.C.: The
Scarecrow Press.

 

Sylven, Christen. 1970. Chylomicron size and its relation
to the composition of dietary fat in the rat. Acta
Physiol. Scan. 79: 516-522.

Tamir, I., D. B. Grant, Audrey S. Fosbrooke, M. M. Segall
and June K. Lloyd. 1968. Effects of a single oral
load of medium-chain triglyceride on serum lipid and
insulin levels in man. J. Lipid Res. 9: 661-666.

Tamir, 1., Susan Gould, Audrey S. Fosbrooke and June K.
Lloyd. 1969. Serum and adipose tissue lipids in
children receiving medium-chain triglyceride diets.
Arch. Dis. Child. 44: 180-186.

Ten-State Nutrition Survey. 1968-1970. U.S. Department of
Health, Education and Welfare. Washington, D. C.

Theuer, Richard C. 1971. Influence of the source of
dietary fat on some metabolic responses of meal-fed
rats. P.S.E.B.M. 36: 765-768.

Wagner, Muriel G. 1970. The irony of affluence. J.A.D.A.
57: 311-315.

Wiley, Joyce H. and G. A. Leveille. 1973. Metabolic
consequences of dietary medium-chain triglycerides in
the rat. J. Nutr. 103; 829—835.

Wiseman, Gerald. 1964. Absorption from the Intestine.
New York: Academic Press.

 

Young, Charlotte M., Sonia Sipin Scanlan, Celia Moodie
Topping, Vladimir Simko and Leo Lutwak. 1971.
Frequency of feeding, weight reduction, and body com-
position. J.A.D.A. 59: 466-471.

 

78

Zucker, Lois M. 1965._ Hereditary obesity in the rat
associated with hyperlipemia. Ann. N.Y. Acad. Sci.
131: 447-458. .

Zurier, Robert B., Robert G. Campbell, Sami A. Hashim and
Theodore B. Van Itallie. 1967. Enrichment of depot
fat with odd and even numbered medium chain fatty
acids. Amer. J. Physiol. 212: 291-294”

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