Role of glucocorticoid in adaptive hyperlipogenesis in the rat.
The effect of glucocorticoid (GC) on the enzyme overshoot response to starvation-refeeding (S-R) and on tritium incorporation into lipids was studied. Long-term effects of hypercortisolism on carcass and liver lipids were also determined. In the first series of experiments, intact, adrenalectomized (ADX) and ADX, GC-replaced rats were either ad libitum fed or starved and refed a 65% glucose diet. Glucose-6-phosphate dehydrogenase and malic enzyme activities in both liver and adipose tissue were determined as were the liver and fat pad lipid levels, hepatic and muscle glycogen content, and in vivo incorporation of 3H (from 3HOH, 1 mCi/100 g b.w.) into liver, adipose tissue and plasma lipids. The role for GC in the enzyme overshoot in S-R rats was reaffirmed as was the effect of ADX on enzyme activity and adipose tissue lipid. Hepatic glycogen content was reduced by adrenalectomy and not reversed by GC replacement in the ad libitum-fed animals. S-R reduced liver glycogen in the intact rats, did not affect liver glycogen in ADX-GC replaced rats and increased liver glycogen in the untreated ADX animals. S-R increased hepatic and adipose tissue lipid synthesis as measured by 3H incorporation. This effect was reduced by ADX and the ADX effect was reversed by GC. Prolonged administration of GC had no effect on increasing hepatic or carcass lipid content of ad libitum-fed animals. Results of these experiments suggest that while ineffective in inducing lipogenesis in ad libitum-fed animals, GC plays a role in the lipogenic response to starvation-refeeding and that this effect is apart from its role in the induction of the enzyme overshoot.