Rat tail suspension causes a decline in insulin receptors

C. A. Stuart, L. S. Kidder, R. A. Pietrzyk, G. L. Klein, D. J. Simmons

Research output: Contribution to journalArticlepeer-review

8 Scopus citations


Decreased muscular activity results in weakness and muscular atrophy. Coincident with this protein catabolic state is glucose intolerance and hyperinsulinemia. Rats were tail suspended for 7 to 14 days to accomplish unloading of the hindlimbs. Insulin resistance was documented in these animals by a 14 day tail suspension-related 26 % increase in serum glucose in spite of a 253 % increase in serum insulin concentration. Microsomal membranes were prepared from hindlimb muscles and specific binding of insulin and insulin-like growth factor I (IGF-I) were determined in these membranes. Insulin binding was decreased by 27 % at 7 days and by 21 % at 14 days. In contrast, IGF-I binding was unchanged at 7 days and was increased by 24 % at 14 days. Liver membrane insulin receptors also had declined by 14 days of suspension, suggesting that the change in insulin receptors was a generalized, humorally-mediated phenomenon. These data suggest that tail suspension in rats results in insulin resistance, hyperinsulinemia, a decline in insulin receptors in liver and muscle, and a relative increase in muscle membrane IGF-I receptors. These data are consistent with the hypothesis that resistance to insulin's effects on protein metabolism in skeletal muscle may contribute to the protein catabolism associated with decreased muscular activity.

Original languageEnglish (US)
Pages (from-to)291-295
Number of pages5
JournalExperimental and Toxicologic Pathology
Issue number5-6
StatePublished - 1993


  • Hyperinsulinemia
  • IGF-I
  • Insulin binding
  • Insulin receptors
  • Insulin resistance
  • Insulin-like growth factor I (IGF-I)
  • Liver, membrane insulin receptors
  • Microsomal membrane
  • Receptors, insulin
  • Skeletal muscle, IGF-I receptors
  • Tail suspension

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