Glycogen synthesis in the perfused liver of adrenalectomized rats.
1. A total loss of capacity for net glycogen synthesis was observed in experiments with the perfused liver of starved adrenalectomized rats. 2. This lesion was corrected by insulin or cortisol in vivo (over 2-5h), but not by any agent tested in perfusion. 3. The activity of glycogen synthetase a, and its increase during perfusion, in the presence of glucose plus glucogenic substrates, were proportional to the rate of net glycogen accumulation. 4. This complete inherent loss of capacity for glycogen synthesis after adrenalectomy is greater than any defect in hepatic metabolism yet reported in this situation, and is not explicable by a decrease in the rate of gluconegenesis (which supports glycogen synthesis in the liver of starved rats). The short-term (2-5h) stimulatory effect of glucocorticoids in the intact animal, on hepatic glycogen deposition, may be mediated partly through insulin action, although neither insulin or cortisol appear to act directly on the liver to stimulate glycogen synthesis.
D000311:Adrenal Glands / Q000502:physiology*; D000315:Adrenalectomy; D000818:Animals; D006006:Glycogen Synthase / Q000378:metabolism; D006601:Hexoses / Q000494:pharmacology; D006854:Hydrocortisone / Q000494:pharmacology; D066298:In Vitro Techniques; D007328:Insulin / Q000172:deficiency / Q000494:pharmacology; D008099:Liver / Q000187:drug effects / Q000378:metabolism*; D008112:Liver Glycogen / Q000096:biosynthesis*; D008297:Male; D006005:Phosphorylases / Q000378:metabolism; D051381:Rats; D013217:Starvation
D006601:Hexoses; D007328:Insulin; D008112:Liver Glycogen; D006005:Phosphorylases; D006006:Glycogen Synthase; D006854:Hydrocortisone