Glycogen metabolism insulin

Insulin appears to activate a process that helps glucose molecules enter the cells of striated muscle and adipose tissue Figure 49-1 depicts normal glucose metabolism. Insulin also stimulates die synthesis of glycogen by die liver. In addition, insulin promotes protein syntiiesis and helps the body store fat by preventing its breakdown for energy. 

Hormones and neuronal activity affect brain glycogen metabolism. Glycogen is affected by hormones endogenous to the brain including vasoactive intestinal peptide and noradrenaline, as well as circulating hormones, such as insulin [61, 63, 64]. The mechanism whereby insulin exerts an effect on glycogen metabolism in brain has not been determined [63]. Glycogen metabolism in brain, unlike in other tissues, is controlled locally, due to differential local metabolic rates. 

Diacylglycerol, on the other hand, is lipid soluble and remains in the lipid bilayer of the membrane. There it can activate protein kinase C (PKC), a very important and widely distributed enzyme which serves many systems through phosphorylation, including neurotransmitters (acetylcholine, a,- and P-adrenoceptors, serotonin), peptide hormones (insulin, epidermal growth hormone, somatomedin), and various cellular functions (glycogen metabolism, muscle activity, structural proteins, etc.), and also interacts with guanylate cyclase. In addition to diacylglycerol, another normal membrane lipid, phos-phatidylserine, is needed for activation of PKC. The DG-IP3 limbs of the pathway usually proceed simultaneously. 

Glycogen metabolism The effects of glucocorticoids on glycogen accumulation appear to be predominantly, although not exclusively, insulin dependent, because glycogen... 

As work with vanadium compounds and diabetes in cell system has continued, it has become clear that there are also insulin-independent mechanisms at work. One insulin-independent signal transduction pathway appears to be involved in glycogen metabolism reactions in rat adipocytes [137] that also involve PI-3K. A major difference was that only vanadate promoted glycogenesis through the activation of a cytosolic protein tyrosine kinase, which was mediated in an insulin receptor-independent manner. 

A. R Saltiel. The paradoxical regulation of protein phosphorylation in insulin action. FASEBJ, 8, (13), 1034-1040, 1994. Also J. A. Printen, M. J. Brady, A. R Saltiel. PTG, a protem phosphatase 1-binding protein with a role in glycogen metabolism. Science, T1S, 1475-1478, 1997. 

Glycogen metabolism in liver is regulated by phosphorylation and dephosphorylation of regulatory and metabolic enzymes. Control of the phosphorylation state is mediated by Ca " ", cAMP, cytosolic glucose concentration, and perhaps, in the case of insulin, by another mechanism. 

Finally, no attempt will be made to review the extensive literature on the influence of various hormones on glycogen metabolism with regard to insulin, the view that its major action is to regulate the permeability of cells to D-glucose, rather than to control the activity of certain enzymes, should not be overlooked. 

The hormone insulin, produced by the pancreas in response to high blood glucose levels, stimulates the synthesis of glycogen, glycogenesis. Insulin is perhaps one of the most influential hormones in the body because it directly alters the metabolism and uptake of glucose in all but a few cells of the body. 

The opposing effects of the hormones insulin and glucagon on glycogen metabolism. 

The effect of insulin on glycogen metabolism is described in Section 21.7. 

Carbohydrate metabolism. Insulin stimulates glycogen synthesis. At the same time it inhibits glycogenolysis and gluconeogenesis. The overall result of these activities is the storage of excess glucose. 

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