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Departamento de Clínica Médica da Universidade Estadual de Campinas, Campinas, Brazil
¹ Departamento de Farmacologia, Instituto de Ciências Biomédicas, Universidade de São Paulo, São Paulo, Brazil
² Departamento de Clínica Médica, Divisão de Nefrologia, Laboratório de Hipertensão Experimental da Faculdade de Medicina da Universidade de São Paulo, São Paulo, Brazil

(Requests for offprints should be addressed to J C Heimann, University of São Paulo School of Medicine, Av. Dr Arnaldo #455, 3^rd floor, Room 3342, 01246-903 São Paulo, SP, Brazil; Email: jheimann{at}usp.br)

^* (P O Prada and M S Coelho contributed equally to this work)

A severe restriction of sodium chloride intake has been associated with insulin resistance and obesity. The molecular mechanisms by which the low salt diet (LS) can induce insulin resistance have not yet been established. The c-jun N-terminal kinase (JNK) activity has been involved in the pathophysiology of obesity and induces insulin resistance by increasing inhibitory IRS-1^ser307 phosphorylation. In this study we have evaluated the regulation of insulin signaling, JNK activation and IRS-1^ser307 phophorylation in liver, muscle and adipose tissue by immunoprecipitation and immunoblotting in rats fed with LS or normal salt diet (NS) during 9 weeks. LS increased body weight, visceral adiposity, blood glucose and plasma insulin levels, induced insulin resistance and did not change blood pressure. In LS rats a decrease in PI3-K/Akt was observed in liver and muscle and an increase in this pathway was seen in adipose tissue. JNK activity and IRS-1^ser307 phosphorylation were higher in insulin-resistant tissues. In summary, the insulin resistance, induced by LS, is tissue-specific and is accompanied by activation of JNK and IRS-1^ser307 phosphorylation. The impairment of the insulin signaling in these tissues, but not in adipose tissue, may lead to increased adiposity and insulin resistance in LS rats.