Ph~stolog~ & Behavior Vol 31, pp 851-855 Pergamon Press Ltd, 1983 Prmted m the U S A

Differential Effects of Medium-

and Long-Chain Triglycerides on Food
Intake of Normal and Diabetic Rats
MARK I FRIEDMAN, NEILE K EDENS AND ISRAEL RAMIREZ

M o n e l l C h e m i c a l S e n s e s C e n t e r , 3500 M a r k e t S t r e e t , P h d a d e l p h t a , P A 19104

Received 6 J u n e 1983

FRIEDMAN, M I , N K EDENS AND I RAMIREZ Differential effetts of medium- and long-tham trtglwertdes on
fi~od mtal, e of normal and d:abette rats PHYSIOL BEHAV 31(6) 851-855, 1983 --Three experiments were performed to
examine the effect of lngesUon of medmm- (MCT) and long-chain (LCT) tnglycerlde ods at the beglnmng of the normal
feeding period on subsequent food retake of normal and diabetic rats In the first experiment, dmbetlc rats reduced food
retake more than normal ammals m the first 6 hr after mgesUon of 2 0 ml of MCT or LCT oll In the second expenment,
diabetic rats reduced food retake to a slmdar extent by 6 hr after mgestlon of 1 5 ml of MCT or LCT od, but the Ume course
of this effect depended on the oll ingested Ingestion of MCT oll produced a decrease m food intake within 2 hr, whereas
ingestion of LCT oll reduced food retake 2-4 hr later In the third experiment, a direct comparison was made of the
differential time course of food retake suppression by MCT or LCT oil m both normal and diabetic rats Diabetic rats
decreased food retake after ingestion of 1 5 ml MCT or LCT oil, whereas normal rats did not Again, m diabetic rats,
ingestion of MCT oll produced a more rapid reduction m food retake than ingestion of LCT oll It is proposed that the more
pronounced reduction m food intake of diabetic rats after oil ingestion Is due to a greater degree of hepatic oxldaUon of
ingested fat, whereas the differential effect of MCT and LCT oil ingestion m diabetic rats is due to a differential rate of
dehvery of the ingested lipid substrate to the hver

Food intake Diabetes Medium-chain tnglycendes Long-chain tnglycendes

P R E V I O U S studies h a v e s h o w n t h a t rats with e x p e r i m e n t a l effect o f fat ingestion, o n e m a y e x p e c t to o b s e r v e d i f f e r e n c e s

d i a b e t e s a l t e r food i n t a k e m o r e d r a m a t i c a l l y t h a n n o r m a l rats
in r e s p o n s e to c h a n g e s in the c o n t e n t o f d i e t a r y fat [3] Re-
d u c t i o n s in the c o n t e n t o f fats in a high-fat diet leads to
p r e d i c t a b l e i n c r e a s e s in f o o d intake in d i a b e t i c rats w h i c h
m a y be t w i c e t h a t o f n o r m a l a n i m a l s [3,4] C o n v e r s e l y , add-
ing fat to a low-fat diet r e d u c e s d i a b e t i c h y p e r p h a g l a , b u t
p r o d u c e s n o c h a n g e in caloric i n t a k e s o f n o r m a l rats [3, 5,
14] T o e x a m i n e this satiating effect o f fat i n g e s t i o n o n food
i n t a k e , e x p e r i m e n t s w e r e p e r f o r m e d in w h i c h d i a b e t i c a n d
n o r m a l rats w e r e fed a small a m o u n t o f p u r e fat at the begin-
nlng o f t h e i r n o r m a l n o c t u r n a l feeding p e n o d a n d s u b s e q u e n t
food i n t a k e s were m o n i t o r e d In c o n t r a s t to d i e t a r y m a n i p u -
lations, this p r o c e d u r e allows for a m o r e direct a s s e s s m e n t of
the effect o f fat c o n s u m p t i o n o n food intake as well as t h e
time c o u r s e o f this effect Also, this p r o c e d u r e a v o i d s t h e
p o t e n t i a l l y c o n f o u n d i n g i n f l u e n c e of c h a n g e s in diet palata-
b l h t y a s s o c i a t e d with a l t e r a t i o n s in food c o n s u m p t i o n
In a d d i t i o n to c o m p a r i n g the effects o f fat i n g e s t i o n o n
food intake in n o r m a l a n d d i a b e t i c rats, the e x p e r i m e n t s de-
s c r i b e d b e l o w also c o m p a r e d the effects o f feeding m e d m m -
( M C T ) a n d long-chain ( L C T ) t n g l y c e n d e oils in o r d e r to ob-
tain insight into t h e m e c h a n i s m b y w h i c h fats r e d u c e food
Intake D i f f e r e n c e s in the digestion, t r a n s p o r t a n d m e t a b o -
h s m o f M C T s a n d L C T s h a v e b e e n w e l l - c h a r a c t e r i z e d [1]
T h e r e f o r e , if a n y o f t h e s e f a c t o r s are i n v o l v e d in the satiating
in the effect o f t h e s e t r l g l y c e n d e s o n food i n t a k e In the
e x p e r i m e n t s r e p o r t e d b e l o w , we find a differential effect of
oll ingestion o n food i n t a k e of n o r m a l a n d diabetic rats and,
in d i a b e t i c a n i m a l s , a differential effect o f M C T a n d L C T oils
as well
GENERAL METHOD
Subjects
Male C D C h a r l e s R i v e r rats ( W i l m i n g t o n , M A ) weighing
250-300 g at t h e time o f s t r e p t o z o t o c m i n j e c t i o n were u s e d
Rats were h o u s e d individually m s t a n d a r d h a n g i n g cages at
a p p r o x i m a t e l y 23°C a n d a d a p t e d to a r e v e r s e d 12/12 h r
d a y / n i g h t lighting s c h e d u l e (lights o u t at 0900 hr) for at least 3
w e e k s p r i o r to testing P u n n a L a b o r a t o r y C h o w a n d tap
w a t e r were available ad lib e x c e p t w h e n n o t e d o t h e r w i s e
Experimental Diabetes
Rats w e r e r a n d o m l y a s s i g n e d to d i a b e t i c o r n o r m a l
g r o u p s D i a b e t e s was i n d u c e d b y Injection o f s t r e p t o z o t o c m
(60 mg/kg, IP m a p H 4 8 citrate buffer) I n j e c t i o n s w e r e
r e p e a t e d if rats did not s h o w p l a s m a glucose levels g r e a t e r
t h a n 22 m M t h r e e d a y s a f t e r InJection T e s t i n g b e g a n 2 - 4
weeks after induction of diabetes

~Thls research was supported by NIH grants AM-31634 and AM-31632

C o p y r i g h t " 1983 P e r g a m o n P r e s s Ltd--0031-9384/83/120851-05503 00

 852 FRIEDMAN, EDENS AND RAMIREZ

40 2 0 ml of s o y b e a n oil ( L C T S i g m a C h e m i c a l Co ), 2 0 ml o f
Normal M C T oil ( M e a d J o h n s o n ) , or n o oll (control) Five m m later
food was r e t u r n e d and i n t a k e s m e a s u r e d 6 and 24 hr later
control T r e a t m e n t s w e r e given m a c o u n t e r b a l a n c e d o r d e r and e a c h
30 ~ LCT oil rat was t e s t e d four t i m e s m e a c h c o n d i t i o n Results pre-
s e n t e d b e l o w r e p r e s e n t the m e a n of the four tests
J MCT o,I
Results

20 As s h o w n in Fig 1, diabetic rats ate more t h a n n o r m a l

A
v o~ 10
¢0
"O Diabetic
o 60
o n o r m a l animals, ingestion of M C T oil did not slgmficantly
LL
40
20
6 hour 24 hour
FIG I Food retake of normal (topl and dmbet~c (bottom) rats 6 and
24 hr after ingestion of 2 0 ml of long- (LCT) or medmm-cham
(MCT) tr|glycende od No od was gwen m control conditions In-
takes were measured starting at the beginning of the mght Values
are means+_S E M of ten rats
Pio( ('dll! C~
Prior to testing, rats were trained to c o n s u m e oil (I 5 or
2 0 ml d e p e n d i n g on the e x p e r i m e n t ) that was placed in an
r e v e r t e d bottle cap a t t a c h e d to the b o t t o m o f t h e i r cage at the
b e g i n n i n g o f the night period Usually 2-3 e x p o s u r e s were
sufficient to p r o d u c e a rapid c o n s u m p t i o n o f o d within 20-30
m m after p r e s e n t a t i o n During training and testing, oil was
given no m o r e t h a n 2-3 t i m e s p e r w e e k with at least o n e day
m w h i c h no oil was g i v e n b e t w e e n tests F o o d intake, cor-
rected for spillage, was m e a s u r e d to the n e a r e s t 0 1 g
Stattstt~ al Anal~ ~ s
D a t a were e v a l u a t e d by an analysis of v a r i a n c e W h e n
slgmficant effects were f o u n d ( p < 0 05), individual c o m p a r i -
s o n s of g r o u p m e a n s were m a d e using S t u d e n t ' s t-test
EXPERIMENT 1
Method
T e n n o r m a l a n d 10 d i a b e t i c rats were used m this experi-
m e n t One hr before the b e g i n n i n g o f the night period, all rats
were d e p r i v e d o f food Fifty rain later rats w e r e given e i t h e r
a n i m a l s during b o t h the 6 and 24 hr periods Oil ingestion
r e d u c e d food intake o f b o t h n o r m a l a n d diabetic rats a f t e r 6
a n d 24 hr of feeding, F ( 2 , 3 6 ) = 19 2, p < 0 001, F(2,36)=45 4,
p < 0 001 Following ingestion o f oil, diabetic rats r e d u c e d
food retake significantly more than n o r m a l a m m a l s by 6 hr,
F ( 2 , 3 6 ) = 5 8, p < 0 001, but not m the s u b s e q u e n t 18 hr,
F ( 2 , 3 6 ) = 0 79, 0 8 > p > 0 2 This difference m r e d u c t i o n o f
g r a m retake was also reflected m d i f f e r e n c e s m p e r c e n t re-
d u c t i o n o f intake f r o m c o n t r o l levels
I n g e s t i o n of M C T or L C T oll p r o d u c e d s l m d a r r e d u c t i o n s
m food retake m diabetic rats after 6 a n d 24 h r o f f e e d m g In
d e c r e a s e food intake f r o m control levels at 6 hr, t ( 9 ) = 2 2
p < 0 05 T h e r e was a t e n d e n c y for food intake at 6 hr to
d e c r e a s e m o r e m n o r m a l rats after ingestion of L C T od than
M C T o11, but this effect was not statistically significant,
t ( 9 ) = 1 2, p < 0 2 By 24 hr food intake o f n o r m a l rats after
ingestion of M C T or L C T ods was r e d u c e d b y s l m d a r
a m o u n t s c o m p a r e d to c o n t r o l levels
EXPERIMENT 2
In the first e x p e r i m e n t diabetic rats s h o w e d a g r e a t e r
r e d u c t i o n m food intake following ingestion o f oll t h a n nor-
mal a m m a l s In o r d e r to c h a r a c t e r i z e the effects o f o d inges-
tion o n food retake m o r e precisely, a n o t h e r e x p e r i m e n t was
p e r f o r m e d m w h i c h food retake o f d | a b e t l c rats was meas-
ured at m o r e f r e q u e n t intervals for 6 h r a f t e r ingestion of
e i t h e r M C T o r L C T oil Only diabetic a n i m a l s were tested,
b e c a u s e n o r m a l rats did not s h o w a reliable d e c r e a s e m food
intake a f t e r M C T oil ingestion In addition, m this experi-
m e n t rats w e r e not g i v e n food until t h e y had c o n s u m e d oil
Method
N i n e diabetic rats were used At the b e g m n l n g o f the night
period (hghts out), rats were depraved o f food for ! hr Rats
were then given 1 5 ml o f od a n d food was r e t u r n e d 30 m m
later All rats had c o n s u m e d t h e od by the time t h e y were
given food In the control c o n d i t i o n , rats were not given oil
a n d food was r e t u r n e d 1 5 hr after d e p r i v a t i o n Food intake
was m e a s u r e d e v e r y 2 h r for the next 6 hr after food was
r e t u r n e d Rats w e r e t e s t e d first with c o r n oil (Sigma Chemi-
cal Co ) a n d t h e n with M C T oll C o n t r o l a n d oll feeding
c o n d i t i o n s were c o u n t e r b a l a n c e d for e a c h test w~th the two
ods
Result~
T h e results o f this e x p e r i m e n t are d i s p l a y e d m Fig 2
F o o d intakes for the t w o control c o n d i t i o n s were not signifi-
c a n t l y different a n d the m e a n o f t h e s e two t e s t s was u s e d
for statistical analysis A s m the first e x p e r i m e n t , diabetic
rats r e d u c e d food i n t a k e s b e l o w control levels after ingestion
o f e i t h e r M C T or L C T oil, F ( 4 , 6 4 ) = 2 2 5, p < 0 001, h o w e v e r ,
the time c o u r s e o f the effect d e p e n d e d on the oil ingested,
T R I G L Y C E R I D E S A N D FOOD I N T A K E 853

I • LCT Normal
• LCT
20 / o MCT /~ o MCT
f -control ~S/~
/ -°'' ~//// 20 - - - Control

Oil
A
c~

fY
v

15
to
"~ 10- t-
° m

"O 10
O
O
u-
5

I I I
2 4 6
,,, I I I
Hours
FIG 2 Food retake of diabetic rats m the first 6 hr of the night
period after ingestion of 1 5 ml of long- (LCT) or medmm-chaln Diabetic
(MCT) triglycerlde od No od was g~ven m control conditions Val-
ues are means-S E M of nine rats
2o ////

F(4,64)=3 6, p < 0 05 After ingestion of MCT oil, rats re-

duced food intake compared to control or L C T conditions in
the first 2 hr of the feeding test, t(8)=5 5 , p < 0 001, compared
to control, t ( 8 ) - 3 5, p < 0 01, compared to LCT, but not in
the two subsequent 2 hr periods When given LCT o11, rats
reduced food intakes compared to the control condition in
the 2-4 hr period of the feeding test, t(8)=2 64, p < 0 05, but
not m the preceedmg or subsequent 2 hr periods
"0
81 0
EXPERIMENT 3 5

In the prewous experiment, diabet]c rats reduced mtakes

more rapidly after ingestion of MCT od than after ingestion
I I , I
of LCT oil However, because rats were tested with MCT oll
after they had been trained to drank and were tested with 2 4 6
LCT oil, the results may have depended on the order of Hours
testing In order to control for any possible order effects, FIG 3 Food intake of normal (top) and dlabenc (bottom) rats m the
another experiment was performed m which rats were given first 6 hr of the mght period after ingestion of 1 5 ml of long- (LCT)
equivalent experience with the two ods prior to testing In or medmm-cham (MCT) tnglycende od No od was given m control
addition, normal rats were used m order to determine conditions Values are means_+S E M of seven normal and eleven
whether they also showed a differential short-term response dmbetlc rats
to MCT and LCT od ingestion

Method normal rats showed no ssgnLficant effect of oll ingestion In

diabetic rats, ingestion of MCT oil reduced food intake com-
Seven normal and 11 diabetic rats were used Procedures
pared to the control condition in the first 2 hr of the feeding
m this experiment were s~mdar to the last except that rats
test, t(10)=3 67, p < 0 01, whereas ingestion of LCT did not
were trained to consume 1 5 ml of a 50 50 mixture of corn off
Ingestion of LCT oil reduced food intake compared to con-
(LCT) and MCT oll prior to testing On test days, each group
of dmbetlc and normal rats were dw]ded into two groups trol conditions in the 2-4 and 4-6 hr periods of the feeding
test, t(10)=2 49, p < 0 05, t(10)=3 07. p < 0 02 Ingestion of
which were fed 1 5 ml of either LCT or MCT oil Control
MCT o11 had no effect on food intake compared to the con-
tests m which no off was given preceded each test with oll
trol condition m the 2-4 period of the feeding test, but de-
Each rat was tested with each oll m a counterbalanced order
creased food intake m the 4-6 hr period, t(10)= 2 58, p <0 05
This greater reduction in gram intake of diabetic rats was
Results
also reflected m a greater percent reduction m intake from
As shown m F]g 3, dmbetlc rats ate more food than nor- control levels
mal ammals during the 6 hr feeding tests, F(1,16)=II 1,
p < 0 01 Ingestion of od reduced food intakes, F(2,32)=8 4,
p < 0 01, and did so more m diabetic than m normal rats. GENERAL DISCUSSION
F(2,32)=3 58, p < 0 05 Separate analys]s of food retake of The results of Experiments 1 and 3 show that ingestion of
 854
od reduces food retake in dmbetlc rats more than normal
animals In Experiment 1, diabetic rats reduced 6 hr food
retakes on a gram basis after oil ingestion 2-5 t~mes more
than normal rats depending on the oil c o n s u m e d In Experi-
ment 3, m which rats ingested less oil (1 5 vs 2 0 ml), normal
rats did not reduce food retake after consuming oil whereas
diabetic animals did It should be noted that the reduction in
food Intake o b s e r v e d after oil ingestion did not appear to be
due to malaise Rats repeatedly c o n s u m e d the small amount
of oil they were given m training and test trials despite the
fact that it reduced their food retake I f m g e s t m g od made the
rats sick, one would expect them to avoid it
In addition to demonstrating a differential effect of oil
ingestion on food intake m normal and dmbettc rats, the
e x p e n m e n t s described a b o v e also revealed a differential ef-
fect of M C T and L C T oil mgestlon on food intake in dlabehc
rats In Experiments 2 and 3, dmbetlc rats reduced food
retake more rapidly after ingesting M C T od than after L C T
oil The largest effect o f M C T od ingestion was observed m
the first 2 hr o f the feedmg test, whereas the reduction m
retakes after L C T oil was c o n s u m e d occurred 2-4 hr after od
ingestion It ~s possible that ingestion of M C T od has longer
lasting effects as well since, in Experiment 3, a suppression
of retake was also o b s e r v e d 4-6 hr after oil consumption
Thus, although ingestion of M C T and L C T otis resulted m
similar decreases in food intake o v e r a 6 hr period, the time
course of this effect depended on the oil c o n s u m e d
Changes m oxtdatlon of metabolic fuels m h v e r have been
imphcated previously m the control of food intake [3,4] It ~s
possible that differences in the hepatic m e t a b o h s m of
medium- ( M C F A ) and long-chain ( L C F A ) fatty acids in nor-
mal and diabetic rats account for the dlfferentml effect of oil
mgeshon on food retake m these animals When msuhn
levels are high, as would be the case m normal rats eating a
high-carbohydrate diet (Purina Chow) at ntght, adipose tis-
sue hpoprotem hpase activity ts increased [13] and most of
the circulating L C T s (chylomtcrons) are taken up into
adipose tissue and are unavadable for oxidation Also, partz-
t~onmg of fatty acids between esterlfiCatlon and oxidation m
hver is controlled in large part by the glucagon insulin raho
[9] When this ratio is low, as would be the case m normal
ammals eating at night, hepatic estenficatton of fatty acids is
p r o m o t e d and their oxidation to ketone bodies and CO., is
inhibited [6] Therefore, under the condtttons of our experi-
ments, relatively httle o f the ingested L C F A would be
oxidized by the liver of normal rats On the other hand m
dmbetes, when lnsuhn levels are low, adipose tissue hpopro-
tern hpase activity ~s low [I0], uptake of hplds ts reduced [12]
and the partitioning of fatty acids m h v e r is shifted toward
oxidation [8,9] Thus, the more pronounced reduction m
food retake of dmbet~cs after ingestion of L C T oil may be due
to the fact that more of the resulting L C F A are oxidized in
hver (see also [11])
Differences m the hepatic utlhZatlon of M C F A may also
underhe the dJfferentml response o f normal and diabetic rats
REFERENCES
Bach A , G Debrv and P Metals Hepatic metaboh~m ot
medmm-cham tnglycendes Bib/Nutr Dteta 25 24-35 1977
Edens N K and M ! Friedman The effect of medlurn- and
long-chain tnglycerldes on food retake m the rat The role of
palatabdlty Paper presented at Eastern Psychological Assooa-
tJon Meeting. 1982
FRIEDMAN EDENS AND RAMIREZ
to MCT od ingestion Experiments with perfused hvers have
shown that M C F A are more ketogenlc m hvers from diabetic
rats than in those from normal rats [8] On the other hand
hvers from normal rats channel more ol the acetyl C o A gen-
erated from oxidation of M C F A into hpogenesls and Kreb s
cycle achvtty than hvers from diabetic rats [8] Thus, mges-
tlon o f either M C T or L C T od probably causes a much
greater flux through the hepatic ketogenlc pathway m dm-
bettc than normal rats These differences in ketogenests or
s o m e related process may account for the increased satiating
effect of oil Ingestion m diabehc rats
The fact that hvers of diabetic rats are maximally
ketogentc [9] and M C T and L C T ods are equally ketogentc m
diabetic rats [2] may explain why mgestlon of M C T and L C T
ods produce similar r e d u c h o n s m food retake o v e r a 6 hr
period tn these ammals H o w e v e r g~ven the similarities in
thetr metabolic fate m diabetes differences m the hepatic
uthzatnon of M C F A and L C F A do not appear to account for
the more rapid effect o f M C T consumption on food mtake m
dmbetlc animals On the other hand differences in the rate of
d e h v e r y of M C F A and L C F A to the liver may p r o w d e an
explanation M C T s are more completely hydrolyzed m the
intestine than LCTs, the resultmg M C F A are absorbed more
proximally in the intestine than L C F A , and, unhke L C F A ,
which are re-estenfied m the mtestlnal wall and are trans-
ported m the form of chylomlcrons to the cwculatJon vm the
lymphatic system, M C F A are not appreciably reestertfied
and are transported d~rectly to the h v e r wa the hepatic portal
veto [1] Thus, m the above experiments, ingestion of M C T
oil may have reduced food mtake m diabetic rats wfthm 2 hr
because it resulted m a rapid increase m hepatic fatty a~ld
oxidation, whereas the effect of L C T otl ingestion was de-
layed because L C F A took longer to reach the hver
In previous studies, Maggio and K o o p m a n s [7] tound that
normal rats decreased food mtake to a s~mllar extent and at a
similar rate after gastric infusions of a hqmd diet containing
either M C T or L C T o~1 Differences m experimental protocol
may account for the differences m thew findmgs and the
present ones F o r example, they used rats that were more
deprived and admmlstered the otis m a mixed hqmd meal of
greater volume via a gastric catheter W h e t h e r any of these
factors underhe the discrepant findings in normal ammals
remains to be determined N e v e r t h e l e s s the present findmgs
are consistent with the results of other studies showing that
food retake m diabetic rats zs more greatly affected by fat
feeding than it is in normal ammals [3 I1] The present re-
sults also extend these findings by showing that fat ingestion
rehably reduces short-term food mtake m d~abet~c rats (see
also [11]) and that the time course of this effect depends on
the chain-length of the fat c o n s u m e d
ACKNOWLEDGEMENTS
The authors thank P Smallman for her techmcal assistance and
J Blescm for typing the manuscript
3 Friedman M l Hyperphagla in rats with experimental diabetes
melhtus A response to a decreased supply of utdlzable fuels I
( o m p P h ~ : o l P ~ w h o 1 9 2 109-117 1978
4 Friedman M l and E M Strlcker The physiological psychol-
ogy of hunger A physiological perspechve P~x~hol Rel 83
40%431 1976
I'RIGLYCERIDES AND FOOD INTAKE
5 Janes, R G and M Prosser Influence of high fat diets on
alloxan diabetes Am J Phystol 151 581-587, 1947
6 Lossow, W J and I L Chalkoff Carbohydrate spanngoffatty
acid oxidation I The relation of fatty acid chmn length to the
degree of spanng II The mechanism by which carbohydrate
spares the oxidation of palmttlc acid Arc h Btot hem Btophvs 57
23-40. 1954
7 Magglo, C A and H S Koopmans Food intake after
mtragastnc meals of short-, medium- or long-chain tnglycende
Phw:ol Behav 28 921-926, 1982
8 McGarry, J D and D W Foster The regulatlonofketogenems
from octanolc a o d J Btol Chem 246 114%1159, 1971
9 McGarry, J D and D W Foster Regulation of hepatic fatty
acid oxidation and ketone body production Ann Rev Bu;t hem
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