Glycogen synthesis by hepatocytes from diabetic rats

Abstract

Hepatocytes prepared from streptozotocin- and alloxan-diabetic rats starved for 24 h contain 0.5--2% wet wt. of glycogen. Glycogen synthesis in the hepatocytes from such rats, after prior depletion of the glycogen by glucagon injection, was studied. As distinct from cells from normal animals, there was no glycogen synthesis from glucose as sole substrate, even at concentrations of 60 mM. When supplied with glucose, a gluconeogenic precursor (lactate, dihydroxyacetone or fructose), and with glutamine there was concurrent synthesis of glucose and of glycogen. Without glutamine there was little or no glycogen synthesis. The rate of glycogen formation was in the same range as for cells from control rats. Glutamine addition markedly activated glycogen synthase in cells of starved diabetic rats, but there was no effect on phosphorylase. We obtained very little synthesis of glycogen with hepatocytes from fed diabetic rats, whereas with normal animals, synthesis by such cells equals or exceeds that obtained from starved rats. The conversion of synthase b (inactive) into the active form was studied in rat liver homogenates. The activation of the synthase in cells from starved diabetic rats is somewhat less than that from normal animals, but that from fed diabetic rats is markedly decreased compared with that in livers of fed control animals or that of starved diabetic animals.

Evaluation of antidiabetic, antihyperlipidemic and antioxidant effects of Boehmeria nivea (L.) Gaudich., Urticaceae, root extract in streptozotocin-induced diabetic rats

“…Because STZ causes selective destruction of β-cells of islets of Langerhans, resulting in a marked decrease in insulin levels, it is rational that glycogen levels in tissues (skeletal muscle and liver) decrease as the influx of glucose in the liver is inhibited in the absence of insulin and recovers on insulin treatment (Vats et al, 2004;Golden et al, 1979;Weber et al, 1966). Our results showed that BNRE supplementation to diabetic rats significantly elevated both muscle and hepatic glycogen contents (Table 5).…”

In vitro reversal of the fasting state of liver metabolism in the rat. Reevaluation of the roles of insulin and glucose.

“…Most of these insulin effects have been small, however, and to our knowledge insulin has never been shown to cause a net accumulation of liver glycogen from glucose or any other substrate. This was certainly the case in the present study and in those described by Golden et al (30) and peripheral tissues. When the diet contained sucrose, fructose would provide an additional source of gluconeogenic carbon.…”

Combined treatment of tetrahydrocurcumin and chlorogenic acid exerts potential antihyperglycemic effect on streptozotocin-nicotinamide-induced diabetic rats

“…Glycogen is the primary intracellular storable form of glucose and its level in various tissues especially in liver and skeletal muscles indicates direct reflection of insulin activity since it regulates glycogen storage by stimulating glycogen synthase and inhibiting glycogen phosphorylase (Golden et al 1979). Because STZ causes destruction of β-cells of islets of Langerhans resulting in marked decrease in insulin levels, the glycogen content in tissues (liver and muscle) decrease as the invasion of glucose in the liver is inhibited in the absence of insulin (Weber et al 1966;Vats et al 2004).…”