Document Detail

Low salt intake modulates insulin signaling, JNK activity and IRS-1ser307 phosphorylation in rat tissues.
MedLine Citation:
PMID:  15930169     Owner:  NLM     Status:  MEDLINE    
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.
Patrícia Oliveira Prada; Michella Soares Coelho; Henrique Gottardello Zecchin; Miriam Sterman Dolnikoff; Alessandra Lia Gasparetti; Luzia Naôko Shinohara Furukawa; Mario José Abdalla Saad; Joel Claudio Heimann
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  The Journal of endocrinology     Volume:  185     ISSN:  0022-0795     ISO Abbreviation:  J. Endocrinol.     Publication Date:  2005 Jun 
Date Detail:
Created Date:  2005-06-02     Completed Date:  2005-07-20     Revised Date:  2009-11-19    
Medline Journal Info:
Nlm Unique ID:  0375363     Medline TA:  J Endocrinol     Country:  England    
Other Details:
Languages:  eng     Pagination:  429-37     Citation Subset:  IM    
Departamento de Clínica Médica da Universidade Estadual de Campinas, Campinas, Brazil.
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MeSH Terms
Adipose Tissue / metabolism
Blood Glucose / analysis
Insulin / blood,  metabolism*
Insulin Receptor Substrate Proteins
Insulin Resistance
JNK Mitogen-Activated Protein Kinases / metabolism*
Liver / metabolism
Muscles / metabolism
Obesity / etiology*,  metabolism
Phosphoproteins / metabolism*
Rats, Wistar
Signal Transduction / drug effects*
Sodium Chloride, Dietary / administration & dosage*
Reg. No./Substance:
0/Blood Glucose; 0/Insulin Receptor Substrate Proteins; 0/Irs1 protein, rat; 0/Phosphoproteins; 0/Sodium Chloride, Dietary; 11061-68-0/Insulin; EC Mitogen-Activated Protein Kinases

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