Please use this identifier to cite or link to this item: http://repositorio.unicamp.br/jspui/handle/REPOSIP/93064
Type: Artigo de periódico
Title: Low Salt Intake Modulates Insulin Signaling, Jnk Activity And Irs-1ser307 Phosphorylation In Rat Tissues
Author: Prada P.O.
Coelho M.S.
Gottardello Zecchin H.
Dolnikoff M.S.
Gasparetti A.L.
Shinohara Furukawa L.N.
Abdalla Saad M.J.
Heimann J.C.
Abstract: 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-1ser307 phosphorylation. In this study we have evaluated the regulation of insulin signaling, JNK activation and IRS-1ser307 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-1ser307 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-1ser307 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. © 2005 Society for Endocrinology.
Editor: 
Rights: fechado
Identifier DOI: 10.1677/joe.1.06028
Address: http://www.scopus.com/inward/record.url?eid=2-s2.0-21244503503&partnerID=40&md5=19f16f8ff23842c648a89975b84c3171
Date Issue: 2005
Appears in Collections:Unicamp - Artigos e Outros Documentos

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