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Journal of Lipid Research, Vol. 10, 395-401, July 1969
Copyright © 1969 by Lipid Research, Inc.
Department of Biochemistry, Vallabhbhai Patel Chest Institute, University of Delhi, Delhi-7, India
Oral administration of vitamin A (30,000 IU daily for 2 days) to young rats caused a marked increase in hepatic glycogen, cholesterol, and glycerides, while hepatic phospholipid content remained almost unaltered.
In an examination of the pathogenesis of the lipid accumulation, it was found that more glucose-14C was incorporated into liver lipids in vitamin A-fed rats, whereas incorporation of glucose-14C and dl-glycine-14C into liver protein remained unaltered. The increase in glucose-14C incorporation was confined to the glyceride-glycerol portion of the lipids; incorporation into liver fatty acids was inhibited. Plasma free fatty acid concentrations were elevated.
It is postulated that in the vitamin A-fed rats, increased accumulation of lipids in the liver is caused by a stimulation of fatty acid mobilization from adipose tissue and enhanced formation of glycerophosphate through glycolysis, with consequent increase in the glyceride synthesis in the liver.
The weight of the adrenals was increased, whereas cholesterol concentration in the gland was decreased, after administration of vitamin A to rats. This indicates adrenocortical stimulation. Interestingly enough, vitamin A feeding did not affect either the level of liver lipids or of plasma FFA in adrenalectomized rats.
Supplementary key words lipid mobilization glyceride-glycerol synthesis adrenal weight cholesterol ascorbic acid adrenalectomy
Submitted on October 15, 1968
Accepted on March 3, 1969
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