Synthesis of liver glycogen in starved alloxan diabetic rats.

Abstract

Alloxan diabetic rats are considered unable to synthesize liver glycogen because of a low activity of glycogen synthetase. The present report shows, however, that livers of alloxan diabetic rats have activities of the I-form of glycogen synthetase intermediate between those of starved normal or adrenalectomized rats, and can synthesize substantial amounts of liver glycogenafter refeeding of a chow diet or administration of hydrocortisone. Neither glycogenic procedure, increased the activity of glycogen synthetase in livers of starved alloxan diabetic rats. In contrast, both normal and adrenalectomized rats had increased activities of the I-form of glycogen synthetase three hours after refeeding. After twenty-four hours of access to food, normal and adrenalectomized rats had liver glycogen contents similar to those found in nonstarved rats, and a markedly decreased activity of synthetase I. Alloxan diabetic rats refed for twenty-four hours also had lowered activity of synthetase I, but the concentration of glycogen was not higher than that found after three hours of refeeding. These results show that livers of alloxan diabetic rats have sufficient glycogen synthetase activity to synthesize glycogen rapidly, but the ability to accumulate larger amounts of glycogen is limited by an alteration in the control of glycogen synthetase activity by the content of liver glycogen. Also, the effect of hydrocortisone on the activity of glycogen synthetase in normal or adrenalectomized rats is the result of insulin release; however, not all the changes in glycogen metabolism produced by adrenalectomy can be explained by insulin deficiency.