Author:
Weber G.,Singhal R. L.,Srivastava S. K.
Abstract
The ability of enzyme-forming systems to meet the challenge of starvation and produce vital metabolites for maintaining homeostasis was studied. The preferential maintenance of hepatic gluconeogenic enzymes in starvation can be blocked by hypophysectomy and also by inhibitors of protein synthesis, actinomycin and ethionine. Starvation, cortisone, and triamcinolone were capable of inducing a pronounced increase in the incorporation of orotate into hepatic RNA. Actinomycin administration blocked the starvation- and steroid-induced rise in RNA specific activity. The glucocorticoid hormone induced increase in enzyme biosynthesis and the rise in free amino acid level were rapidly blocked by actinomycin and ethionine and were affected also by starvation.In the adaptation of the organism to acute starvation the hepatic enzyme-forming systems are regulated by the interplay of two hormones to produce a preferential maintenance of key gluconeogenic enzymes. Insulin, a suppressor of biosynthesis of gluconeogenic enzymes, is known to decrease in amount during starvation. Under the same circumstances glucocorticoid hormones, which are inducers of the biosynthesis of gluconeogenic enzymes, are present and thought to be responsible for the preferential maintenance of key gluconeogenic enzyme activities, thus ensuring adequate blood glucose levels in starvation.
Publisher
Canadian Science Publishing
Cited by
9 articles.
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