title: Regulation of cardiac glycogen synthase.
abstract: In perfused rat hearts insulin can activate, and catecholamines can inactivate, glycogen synthase (EC 2.4.1.11); the magnitude of each hormonal response is magnified if tissue glycogen levels are depleted. Both beta-adrenergic and alpha-adrenergic agonists inactivate insulin-stimulated and basal glycogen synthase, with each promoting the same extent of inactivation in both circumstances. In this system beta-adrenergic agonists act via cyclic AMP (cAMP), and alpha-adrenergic agonists via Ca2+, whereas insulin action appears to be independent of either cAMP or Ca2+. The action on cardiac glycogen synthase by the physiological catecholamine epinephrine is apparently mediated by the concomitant interaction with both alpha and beta receptors; interaction with each is mediated by their separate second messenger systems, which combine to produce the end physiological response.
mesh_terms: D000818:Animals; D002118:Calcium / Q000502:physiology; D002395:Catecholamines / Q000502:physiology; D000242:Cyclic AMP / Q000502:physiology; D004789:Enzyme Activation / Q000187:drug effects; D006006:Glycogen Synthase / Q000037:antagonists & inhibitors / Q000378:metabolism*; D007328:Insulin / Q000502:physiology; D009206:Myocardium / Q000201:enzymology*; D010766:Phosphorylation; D011494:Protein Kinases / Q000378:metabolism; D051381:Rats; D011941:Receptors, Adrenergic / Q000502:physiology
chemical_list: D002395:Catecholamines; D007328:Insulin; D011941:Receptors, Adrenergic; D000242:Cyclic AMP; D006006:Glycogen Synthase; D011494:Protein Kinases; D002118:Calcium