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Article

Magnesium Deficiency Modulates the Insulin Signaling Pathway in Liver but Not Muscle of Rats¹

Marise A. B. Reis, Felix G. R. Reyes^*2, Mário J. A. Saad and Lício A. Velloso

Departamento de Fisiologia e Biofísica, Instituto de Biologia, Universidade Estadual de Campinas (UNICAMP), CEP 13083–970, Campinas, São Paulo, Brazil; ^* Departamento de Ciência de Alimentos, Faculdade de Engenharia de Alimentos, Universidade Estadual de Campinas (UNICAMP), CP 6121, CEP 13081–970, Campinas, São Paulo, Brazil; and Departamento de Clínica Médica, Faculdade de Ciências Médicas, Universidade Estadual de Campinas (UNICAMP), CEP 13081–970, Campinas, São Paulo, Brazil.

²To whom correspondence should be addressed.

Altered insulin secretion and sensitivity have been observed in Mg-deficient animals. However, the effects of Mg deficiency and supplementation on intracellular signaling events triggered by insulin are unknown. Therefore, we studied the early steps of insulin action in muscle and liver of rats fed Mg-deficient (DF-6, DF-11) or control (CO-6, CO-11) diets for 6 or 11 wk, respectively, and Mg-deficient or control diets for 6 wk, followed by Mg supplementation for 5 wk (SDF and SCO groups, respectively). There were no differences in the glucose disappearance rate (K_itt) or insulin signaling between CO-6 and DF-6 rats. Between the two groups of rats fed for 11 wk, the DF-11 group had a significantly greater K_itt. SDF and SCO rats had K_itt that did not differ from CO-11 rats, but that were significantly lower than in DF-11 rats. In the latter rats, insulin receptor and insulin receptor substrate-1 protein and phosphorylation levels were elevated in liver and there was a greater association between the insulin receptor substrate-1 and p85 subunit of phosphatidylinositol 3-kinase compared with CO-11 rats. There were no differences in the early steps of insulin action in SDF and control rats. These results suggest that the normal insulin sensitivity maintained by Mg supplementation and the increased insulin sensitivity produced by a long period of Mg deprivation may result, at least in part, from alterations in or maintenance of the early molecular steps of insulin action in hepatic tissue.

KEY WORDS: • insulin receptor • insulin receptor substrate-1 • magnesium deficiency • magnesium supplementation • rats

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