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Am J Physiol Endocrinol Metab 279: E1235-E1241, 2000;
0193-1849/00 $5.00
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Vol. 279, Issue 6, E1235-E1241, December 2000

Immobilization depresses insulin signaling in skeletal muscle

Munetaka Hirose, Masao Kaneki, Hiroki Sugita, Shingo Yasuhara, and J. A. Jeevendra Martyn

Department of Anesthesia and Critical Care, Harvard Medical School, and Anesthesia Services, Massachusetts General Hospital and Shriners Hospital for Children, Boston, Massachusetts 02114

Prolonged immobilization depresses insulin-induced glucose transport in skeletal muscle and leads to a catabolic state in the affected areas, with resultant muscle wasting. To elucidate the altered intracellular mechanisms involved in the insulin resistance, we examined insulin-stimulated tyrosine phosphorylation of the insulin receptor beta -subunit (IR-beta ) and insulin receptor substrate (IRS)-1 and activation of its further downstream molecule, phosphatidylinositol 3-kinase (PI 3-K), after unilateral hindlimb immobilization in the rat. The contralateral hindlimb served as control. After 7 days of immobilization of the rat, insulin was injected into the portal vein, and tibialis anterior muscles on both sides were extracted. Immobilization reduced insulin-stimulated tyrosine phosphorylation of IR-beta and IRS-1. Insulin-stimulated binding of IRS-1 to p85, the regulatory subunit of PI 3-K, and IRS-1-associated PI 3-K activity were also decreased in the immobilized hindlimb. Although IR-beta and p85 protein levels were unchanged, IRS-1 protein expression was downregulated by immobilization. Thus prolonged immobilization may cause depression of insulin-stimulated glucose transport in skeletal muscle by altering insulin action at multiple points, including the tyrosine phosphorylation, protein expression, and activation of essential components of insulin signaling pathways.

insulin receptor; insulin resistance; insulin receptor substrate-1; muscle wasting; phosphatidylinositol 3-kinase


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