Differential regulation of glycogen synthase activity by insulin and glucose in vivo in individual skeletal muscles of the rat. Sugden, Mary C., Mark J. Holness, and Lee G. D. Fryer. Department of Biochemistry, Basic Medical Sciences, St Bartholomew's and the Royal London School of Medicine and Dentistry Queen Mary and Westfield College, University of London, London, U.K.
APStracts 4:0107E, 1997.
G6P-independent GS (GSa) and GS total activities were measured in muscles from 24 h-starved rats. Intravenous glucose tolerance tests (0.5g/kg body weight) were used to produce physiological, transient increases in insulin and glucose concentrations. GS activation occurred at AF10 minutes after glucose administration with peak activation at AF15 min. GS activation was reversed at AF15 min after insulin and glucose concentrations had returned to basal. No differences existed between fast- and slow-twitch muscles. Hyperinsulinemia (AF160 mU/ml) in the absence of hyperglycemia elicited 1.5-fold activation of GS (P<0.001) in 2 of 3 fast-twitch muscles, but did not activate GS in slow-twitch muscles. Glucose infusion (glycemia AF8 mM; insulin AF40 mU/ml) significantly (P<0.01) increased %GSa in 4 of the 5 muscles. Hyperglycemia with modest hyperinsulinemia evoked greater enhancement of GSa activity in fast-twitch muscle than insulin alone at a higher concentration (P<0.01). In summary, hyperinsulinemia without hyperglycemia does not result in maximal activation of GS in fast-twitch muscle and a rise in glycemia is obligatory for GS activation by insulin in slow -twitch muscle. The data support an important role for glycemia in modulating the response of skeletal-muscle GS to insulin and provide further evidence of heterogeneity between skeletal-muscle types. 

Received 14 January 1997; accepted in final form 23 April 1997.
APS Manuscript Number E22-7.
Article publication pending Am. J. Physiol. (Endocrinol. Metab.).
ISSN 1080-4757 Copyright 1997 The American Physiological Society.
Published in APStracts on 13 May 1997