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Metabolism of genetically obese rats on normal or high-fat diet
Metabolism of Genetically Obese Rats on N o r m a l or H i g h - F a t Diet
D. Lemonnier 0
R. Aubert 0
J.-P. Suquet 0
G. Rosselin 0
0 Laboratoire de Nutrition Humaine de l'Institut Scientifique et Technique de l'Alimentation, et Unit6 de Recherche de Diab6tologie et d'Etudes Radioimmunologiques des I-Iormones Prot6iques, U.55 I.N.S.E.R.M. , Paris , France
Summary. Adult genetically obese fafa rats showed a high level of lipogenesis from glucose in liver but not in adipose tissue; pancreatic content and serum levels of insulin were elevated. Glucose uptake anO insulin sensitivity were decreased in muscle, fafa rats and their lean littermates fed a high-fat diet showed increased fat deposits. Serum insulin levels were not significantly affected by diet in either group. The larger the fat cells were, the more actively they utilised glucose; insulin sensitivity was influenced both by diet and cell size. Control rats made obese by a high caloric diet did not show insulin resistance in muscle. -- The data indicate that in adult obesity in these rats, even in the presence of marked hyperinsulinism, increased lipogenesis in adipose tissue is not a prerequisite. Rather, fat storage is a consequence of increased uptake of circulating triglycerides. On a diet rich in carbohydrate, adipose tissue fatty acids were mainly of hepatic origin; on a high-fat diet they were of dietary origin.
High-fat diet; rat; nutritional obesity; genetic obesity; adipose tissue; liver; muscle metabolism; insulin sensitivity; pancreatic glucagon; pancreatic and plasmatic insulin
-
Obesity is associated with hyperinsulinism i.e.
increased insulin secretion and high plasma insulin
levels. This hyperinsulinism is partly related to a high
carbohydrate intake [l]. Long term feeding of a high
fat diet to genetically obese obob mice (a) markedly
increases their obesity, (b) has no effect on their
hyperglycemia, but (c) decreases serum insulin levels [
2
].
Moreover, obesity can be induced in lean animals b y
feeding a high-fat-low-carbohydrate diet given ad lib.
[
3
]. This kind of experimental obesity is characterized
b y normal levels of circulating insulin in vivo, and i n
vitro b y a decreased insulin response to glucose [
4
].
These data indicate t h a t obesity per #e is not closely
related to hyperinsulinism.
I n the present investigation, genetically obese f a f a
rats were studied. They are known to present with a
high degree of hyperinsulinism [
5, 6
], high levels of
serum lipids [7] and an elevated lipogenesis of adipose
tissue [
8
]. The aim of the study was to investigate the
Materials and Methods
Five m o n t h old male genetically obese f a f a rats [
7
]
and their lean littermates (FaFa or Fafa) were fed ad
lib for 7 months either a control diet T (9% of calories
as lipid, 22% as protein, and 69% as carbohydrate), or
a high-fat (72% of calories as lipid, 22% as protein,
and 16% as carbohydrate) diet S [
3
]. Four groups of
rats were obtained. Animals were killed b y deeapita- 9
tion in the fed state in the morning. Blood was
collected and serum glucose was assayed b y the glucose
oxidase method (Boehringer Mannheim Test). Serum
insulin was measured by the method of Rosselin et al.
[
9
]. The pancreatic content of insulin was determined as
previously described [
4
]. Pancreatic glueagon was
assayed according to Jarrousse et al. [
10
].
The incorporation of glueose-U14C into C02, lipids
or glycogen in liver slices, hemidiaphragms and
periGroups
Fa T
Fa S
f a T
fa S
Body
weight
(g)
5 3 0 = ~ 1 2 . 2
5664-16.1
672i36.4
885-L31.0 b
Serum
glucose
(mg/lOO ml)
132~=5.6
119
134-4-4.7
121-4-3.1
Serum
insulin
(vU/ml)
138 1 1 . 5
167 42.3
536~= 101
422~= 6 9 . 9
Pancreatic
weight
(nag)
14044-77.7
1 3 4 1 = = 6 5 . 2
1 3 1 4 = ~ 9 7 . 5
1 4 1 4 ~ = 6 4 . 0
Stored insulin Stored glucagon
(U per pancreas) (~zgper
pancreas)
1.85+0.149 8.37
1.48~0.185 7.06
3.22~0.549 5.22i0.400
3.15 6.58=[=0.38a6
locus of fat synthesis in the obese animals and their
lean littermates, and the possible influence of different
diets. Special attention was given to the role of insulin
and of fat cell size in this model of hereditary and/or
dietary obesity.
genital adipose tissue pieces, was measured as described
elsewhere [i1]. Insulin (1 mU/ml) was added to the
incubation medium in the case of adipose tissue and
muscle. Measurements of adipose tissue cellularity
have been described [
3
].
D. Lemonnier et al. : Metabolism of Genetically Obese l~ats on Normal or High-Fat Diet
Body weight was significantly increased b y the
combination of high-fat diet and the obesity genes of
fafa rats (Table 1).
Serum glucose tended to decrease slightly in rats on
high fat diet. Pooling obese (fafa) and nonobese (FaFa)
t y p e rats, the high fat diet reduced blood glucose levels
significantly ( p ~ 0.01). Serum insulin was not
significantly changed b y high fat diet. The most striking
observation was a four-fold increase in circulating
in (...truncated)