The effects of acute (24 h) and chronic (5 weeks) hindlimb suspension on insulin-stimulated glucose utilization by the rat soleus muscle were studied in vitro. Hindlimb suspension resulted in an enhancement of basal glucose transport, lactate production, and glycogen synthesis. An increase in the sensitivity of these processes to insulin occurred as early as 24 h and persisted for 5 weeks of the muscle unloading. An increased responsiveness to insulin was found only for glucose transport after 24 h. The present data do not support the concept that the enhanced glucose utilization and improved muscle insulin sensitivity during hindlimb suspension are related to muscle atrophy, which is not observed in the early stage of muscle unweighting.
Biological actions of GH on muscle growth and metabolism are mediated through specific trans-membrane receptors. The aim of this study was to determine GH receptor (GHR) mRNA expression in muscle atrophy. GHR gene expression in the rat was investigated by in situ hybridization and RT-PCR in slow-twitch oxidative muscle [soleus (SOL)] and fast-twitch glycolytic muscle [extensor digitorum longus (EDL)] after 7 and 35 d of hindlimb unloading. In control rats, the RT-PCR mRNAs levels of GHR were greater (+34%) in EDL compared with SOL. At single fiber level, relative expression of GHR mRNA increases in the following order: IIb>IIa>I. After hindlimb unloading, GHR expression significantly increased in atrophied SOL muscle after 7 (+170%) and 35 (+220%) d, whereas no significant alterations appeared in the EDL muscle. At the individual fiber level, in situ hybridization demonstrated this increase was accounted for by an increase in type I fiber expression of GHR transcripts. This increase was also seen in the EDL, but the low content of type I fibers in EDL resulted in a nonsignificant increase in GHR transcript content. The present data suggest that muscle atrophy is associated with a muscle fiber type-specific GHR mRNA up-regulation mechanism that helps protect atrophying fibers in EDL but might be part of an attempt to repair in SOL.
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