Rats that are made insulin resistant by glucosamine treatment have impaired skeletal muscle insulin receptor phosphorylation

D. Spampinato, A. Giaccari, V. Trischitta, B. V. Costanzo, L. Morviducci, A. Buongiorno, U. Di Mario, R. Vigneri, Lucia Frittitta

Research output: Contribution to journalArticlepeer-review

Abstract

The current study sought to verify whether glucosamine (GlcN)-induced insulin resistance is associated with impaired insulin receptor (IR) autophosphorylation. Rats were given either saline or primed continuous GlcN infusion (5 μmol.kg-1.min-1) 10 minutes prior to and during euglycemic hyperinsulinemic clamp (primed continuous infusion of 20 mU.kg-1.min-1 insulin for 2 hours). IR autophosphorylation was measured in skeletal muscle after in vivo insulin stimulation (ie, during clamp) by Western blot and then retested after subsequent in vitro 0.1 to 100 nmol/L insulin stimulation (by enzyme-linked immunosorbent assay [ELISA]). Tissue PC-1 enzymatic activity was also measured. In vivo, insulin/GlcN rats had decreased (P <.01) whole body glucose uptake (37.7 ± 2.1 v 49.7 ± 2.7 mg.kg-1.min-1 in respect to insulin/saline), receptor autophosphorylation (37 ± 5 v 82 ± .0 arbitrary units/mg protein), and insulin receptor substrate-1 (IRS-1) phosphorylation (112% ± 15% v 198% ± 23% of saline infusion rats). Receptor autophosphorylation was correlated with whole body glucose uptake (r = 0.62, P <.05). Skeletal muscle PC-1 activity (58.8 ± 10.7 v 55.7 ± 5.8 nmol.mg-1.min-1) was not different in the 2 groups. Our data show that GlcN-induced insulin resistance is mediated, at least in part, by impaired skeletal muscle IR autophosphorylation.

Original languageEnglish
Pages (from-to)1092-1095
Number of pages4
JournalMetabolism
Volume52
Issue number9
DOIs
Publication statusPublished - Sep 1 2003

ASJC Scopus subject areas

  • Endocrinology
  • Endocrinology, Diabetes and Metabolism

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