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Rats with monosodium glutamate-induced obesity and insulin resistance exhibit low expression of Galpha(i2) G-protein.

Abstract
In order to test the potential role of inhibitory G-proteins in mechanisms of insulin resistance in adipose tissue of obese animals we determined the content of Galpha(i1) and Galpha(i2) proteins and an extent of protein tyrosine phosphorylation in epididymal fat tissue cell membranes using immunoblot. Monosodium glutamate-induced obese rats displayed adipose tissue hypertrophy, elevated levels of insulin, leptin and slightly elevated serum glucose. We found significantly decreased protein content of Galpha(i2) in adipose tissue plasma membranes of obese rats. This was in accordance with lower protein tyrosine phosphorylation noticed in adipose tissue cell homogenate of glutamate-treated animals. Our results confirm the role of Galpha(i2) in development of insulin resistance by crosstalk between the reduced level of inhibitory G-protein and insulin receptor mediated most likely by activation of phosphotyrosine protein dephosphorylation.
AuthorsM Baculikova, R Fiala, D Jezova, L Macho, S Zorad
JournalGeneral physiology and biophysics (Gen Physiol Biophys) Vol. 27 Issue 3 Pg. 222-6 (Sep 2008) ISSN: 0231-5882 [Print] Slovakia
PMID18981538 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • Phosphotyrosine
  • GTP-Binding Protein alpha Subunit, Gi2
  • Sodium Glutamate
Topics
  • Adipocytes (cytology)
  • Animals
  • Cell Membrane (metabolism)
  • Down-Regulation (drug effects)
  • GTP-Binding Protein alpha Subunit, Gi2 (metabolism)
  • Insulin Resistance
  • Male
  • Obesity (chemically induced, metabolism)
  • Phosphotyrosine (metabolism)
  • Rats
  • Rats, Sprague-Dawley
  • Sodium Glutamate (toxicity)

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