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This version published online on December 23, 2004
Endocrinology, doi:10.1210/en.2004-0906
A more recent version of this article appeared on April 1, 2005
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Submitted on July 14, 2004
Accepted on December 3, 2004

Intact insulin and insulin-like growth factor -I receptor signaling is required for growth hormone effects on skeletal muscle growth and function in vivo

Hyunsook Kim, Elisabeth Barton, Naser Muja, Shoshana Yakar, Patricia Pennisi, and Derek LeRoith*

Diabetes Branch, National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), National Institutes of Health, Bethesda, Maryland 20892; Anatomy and Cell Biology, University of Pennsylvania SDM, Philadelphia, PA; National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD

* To whom correspondence should be addressed. E-mail: Derek{at}helix.nih.gov.

Growth hormone (GH) and insulin-like growth factor-1 (IGF-1) are potent regulators of muscle growth and function. Although IGF-1 is known to mediate many of the effects of GH, it is not yet clear whether all effects of GH are completely dependent on the IGF-1 system. To evaluate the biological effects of the GH/IGF-1 axis on muscle growth, we administrated rhGH to mice, which lack IGF-1 function specifically in skeletal muscle, due to the overexpression of a dominant negative IGF-1 receptor in this tissue (MKR mice). GH treatment significantly increased the levels of hepatic IGF-I mRNA and serum IGF-I levels in both wild-type (WT) and MKR mice. These GH-induced effects were paralleled by increases in body weight and in the weights of most GH-responsive organs in both groups of mice. Interestingly, unlike WT mice, GH treatment had no effect on skeletal muscle weight in MKR mice. GH treatment failed to reverse the impaired muscle function in MKR mice. Furthermore, MKR mice exhibited no effects of GH on the cross-sectional area of myofibers and the proliferation of satellite cells. Taken together, these data suggest that the in vivo effects of GH on muscle mass and strength are primarily mediated by activation of the IGF-1 receptor.




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