Please use this identifier to cite or link to this item: http://repositorio.unicamp.br/jspui/handle/REPOSIP/52747
Type: Artigo de periódico
Title: Low salt intake modulates insulin signaling, JNK activity and IRS-1(ser307) phosphorylation in rat tissues
Author: Prada, PO
Coelho, MS
Zecchin, HG
Dolnikoff, MS
Lia Gasparetti, A
Furukawa, LNS
Saad, MJA
Heimann, JC
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-1(ser307) phosphorylation. In this study we have evaluated the regulation of insulin signaling, JNK activation and IRS-1(ser307) 7 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.
Country: Inglaterra
Editor: Soc Endocrinology
Rights: fechado
Identifier DOI: 10.1677/joe.1.06028
Date Issue: 2005
Appears in Collections:Artigos e Materiais de Revistas Científicas - Unicamp

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