Lipogenesis in the genetically obese Zucker rat
Lipogenesis in the genetically obese Zucker rat
In situ fatty acid synthesis has been measured with 3H20 in lean and obese Zucker (fa/fa) rats. The accumulation of fatty acids was increased in both the liver and adipose tissue of young fa/fa rats as a result of both an increased rate of lipogenesis and an increase in tissue mass. Whereas total hepatic lipogenesis increased with age, total adipose tissue lipogenesis decreased in older fa/fa rats. Experiments with hepatectomized rats showed that the liver was the major site of the excess fatty acid synthesis in the fa/fa rats. The enhanced rate of lipogenesis in fa/fa rats was abolished by either pair feeding or streptozotocin treatment. The results suggest that the increased fatty acid synthesis in fa/fa rats is secondary to the hyperphagin, hyperinsulinaemia and increased mass of hepatic and adipose tissues. Sucrose feeding resulted in an increased hepatic and adipose tissue lipogenesis and in insulin levels in lean animals with an increase in hepatic lipogenesis and insulin levels in the fa/fa rats. Adrenalectomy decreased the rates of lipogenesis in both the liver and adipose tissues, insulin levels and weight gain of fa/fa rats.Pre-obese fatty rats have been identified by their lower rectal temperature (34.6 + 0.2°C v 35.4 + 0.3°C) from day 16 onwards. Hepatic lipogenesis, hepatic glucose-6-phosphate dehydrogenase, hepatic acetylCoA carboxylase and insulin levels remained unchanged in suckling pre-obese rats and increased only after weaning when all the values for the obese were significantly different from values obtained for lean rats. However, adipose tissue lipogenesis, glucose-6-phosphate dehydrogenase, acetylCoA-carboxylase and adipocyte size were all significantly increased in.the pre-obese suckling rats from day 10 onwards. The results suggest that the primary genetic defect in the fatty rats may be related to either a defective thermogenic process or a defective control of adipose tissue lipogenesis.
University of Southampton
Godbole, V.Y
c3205689-281f-4f47-a735-32aaee5080a8
1978
Godbole, V.Y
c3205689-281f-4f47-a735-32aaee5080a8
Godbole, V.Y
(1978)
Lipogenesis in the genetically obese Zucker rat.
University of Southampton, Doctoral Thesis.
Record type:
Thesis
(Doctoral)
Abstract
In situ fatty acid synthesis has been measured with 3H20 in lean and obese Zucker (fa/fa) rats. The accumulation of fatty acids was increased in both the liver and adipose tissue of young fa/fa rats as a result of both an increased rate of lipogenesis and an increase in tissue mass. Whereas total hepatic lipogenesis increased with age, total adipose tissue lipogenesis decreased in older fa/fa rats. Experiments with hepatectomized rats showed that the liver was the major site of the excess fatty acid synthesis in the fa/fa rats. The enhanced rate of lipogenesis in fa/fa rats was abolished by either pair feeding or streptozotocin treatment. The results suggest that the increased fatty acid synthesis in fa/fa rats is secondary to the hyperphagin, hyperinsulinaemia and increased mass of hepatic and adipose tissues. Sucrose feeding resulted in an increased hepatic and adipose tissue lipogenesis and in insulin levels in lean animals with an increase in hepatic lipogenesis and insulin levels in the fa/fa rats. Adrenalectomy decreased the rates of lipogenesis in both the liver and adipose tissues, insulin levels and weight gain of fa/fa rats.Pre-obese fatty rats have been identified by their lower rectal temperature (34.6 + 0.2°C v 35.4 + 0.3°C) from day 16 onwards. Hepatic lipogenesis, hepatic glucose-6-phosphate dehydrogenase, hepatic acetylCoA carboxylase and insulin levels remained unchanged in suckling pre-obese rats and increased only after weaning when all the values for the obese were significantly different from values obtained for lean rats. However, adipose tissue lipogenesis, glucose-6-phosphate dehydrogenase, acetylCoA-carboxylase and adipocyte size were all significantly increased in.the pre-obese suckling rats from day 10 onwards. The results suggest that the primary genetic defect in the fatty rats may be related to either a defective thermogenic process or a defective control of adipose tissue lipogenesis.
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Published date: 1978
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Local EPrints ID: 463906
URI: http://eprints.soton.ac.uk/id/eprint/463906
PURE UUID: db4864eb-7432-44f3-adde-bf2db8435179
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Date deposited: 04 Jul 2022 20:58
Last modified: 16 Mar 2024 19:06
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Author:
V.Y Godbole
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