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Articles in PresS, published online ahead of print February 5, 2002
Am J Physiol Endocrinol Metab, 10.1152/ajpendo.00254.2001
Submitted on June 13, 2001
Accepted on February 4, 2002
1 Internal Medicine, Washington University School of Medicine, St. Louis, MO, USA
* To whom correspondence should be addressed. E-mail: fisherjs{at}slu.edu.
We varied rates of glucose transport and glycogen synthase (GS) activity in isolated rat epitrochlearis muscle to examine the role of each process in determining the rate of glycogen accumulation. GS activity (GSI%) was maintained at or above the fasting, basal range during 3 h of incubation with 36 mM glucose and 60 µU/ml insulin. Lithium (2 mM LiCl) added to insulin increased glucose transport rate and muscle glycogen content compared with insulin alone. The glycogen synthase kinase-3ß inhibitor GF109203x (10 µM, GF) maintained GSI% ~2-fold higher than insulin ± lithium but did not increase glycogen accumulation. When GSI% was lowered below the fasting range by prolonged incubation with 36 mM glucose and 2 mU/mL insulin, raising rates of glucose transport with bpV(phen) or of GSI% with GF produced additive increases in glycogen concentration. Phosphorylase activiity was unaffected by GF or bpV(phen). In muscles of fed animals, GSI% was ~30% lower than in those of fasted rats, and insulin-stimulated glycogen accumulation did not occur unless GSI% was raised with GF. We conclude that the rate of glucose transport is rate limiting for glycogen accumulation unless GSI% is below the fasting range, in which case both glucose transport rate and GS activity can limit glycogen accumulation.
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