Contraction activates glucose uptake and glycogen synthase normally in muscles from dexamethasone-treated rats

Glucocorticoids cause insulin resistance in skeletal muscle. The aims of the present study were to investigate the effects of contraction on glucose uptake, insulin signaling, and regulation of glycogen synthesis in skeletal muscles from rats treated with the glucocorticoid analog dexamethasone (1 m...

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Bibliographic Details
Published in:American journal of physiology: endocrinology and metabolism 2005-08, Vol.52 (2), p.241-250
Main Authors: RUZZIN, Jérome, JENSEN, Jørgen
Format: Article
Language:English
Subjects:
Biological and medical sciences
Fundamental and applied biological sciences. Psychology
Glucose
Hormones
Insulin
Muscular system
Rodents
Vertebrates: endocrinology
Online Access:Get full text
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Summary:Glucocorticoids cause insulin resistance in skeletal muscle. The aims of the present study were to investigate the effects of contraction on glucose uptake, insulin signaling, and regulation of glycogen synthesis in skeletal muscles from rats treated with the glucocorticoid analog dexamethasone (1 mg x kg-1 x day-1 ip for 12 days). Insulin resistance in dexamethasone-treated rats was confirmed by reduced insulin-stimulated glucose uptake (35%), glycogen synthesis (70%), glycogen synthase activation (80%), and PKB Ser473 phosphorylation (40%). Chronic dexamethasone treatment did not impair glucose uptake during contraction in soleus or epitrochlearis muscles. In epitrochlearis (but not in soleus), the presence of insulin during contraction enhanced glucose uptake to similar levels in control and dexamethasone-treated rats. Contraction also increased glycogen synthase fractional activity and dephosphorylated glycogen synthase at Ser645, Ser649, Ser653, and Ser657 normally in muscles from dexamethasone-treated rats. After contraction, insulin-stimulated glycogen synthesis was completely restored in epitrochlearis and improved in soleus from dexamethasone-treated rats. Contraction did not increase insulin-stimulated PKB Ser473 or glycogen synthase kinase-3 (GSK-3) phosphorylation. Instead, contraction increased GSK-3 Ser9 phosphorylation in epitrochlearis (but not in soleus) in muscles from control and dexamethasone-treated rats. In conclusion, contraction stimulates glucose uptake normally in dexamethasone-induced insulin resistant muscles. After contraction, insulin's ability to stimulate glycogen synthesis was completely restored in epitrochlearis and improved in soleus from dexamethasone-treated rats. [PUBLICATION ABSTRACT]
ISSN:0193-1849
1522-1555