Aspirin inhibits serine phosphorylation of IRS-1 in muscle and adipose tissue of septic rats

Whole body insulin resistance has been demonstrated in septic patients and in infected animals. In this study, we demonstrate that sepsis induces insulin resistance and that pretreatment with aspirin inhibits sepsis-induced insulin resistance. Sepsis was observed to lead to serine phosphorylation of...

Full description

Saved in:
Bibliographic Details
Published in:Biochemical and biophysical research communications 2004-07, Vol.320 (3), p.992-997
Main Authors: Barreiro, Guilherme C, Prattali, Raphael R, Caliseo, Caio T, Fugiwara, Felipe Y, Ueno, Mirian, Prada, Patrı́cia O, Velloso, Lı́cio A, Saad, Mario J.A, Carvalheira, José B.C
Format: Article
Language:English
Subjects:
Adipose Tissue - metabolism
Animals
Aspirin - pharmacology
Insulin
Insulin Receptor Substrate Proteins
Insulin Resistance
Male
Mitogen-activated protein kinase
Muscle, Skeletal - drug effects
Muscle, Skeletal - metabolism
Phosphoproteins - metabolism
Phosphorylation - drug effects
Rats
Rats, Wistar
Sepsis
Sepsis - metabolism
Serine - metabolism
Tyrosine phosphorylation
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Whole body insulin resistance has been demonstrated in septic patients and in infected animals. In this study, we demonstrate that sepsis induces insulin resistance and that pretreatment with aspirin inhibits sepsis-induced insulin resistance. Sepsis was observed to lead to serine phosphorylation of IRS-1, a phenomenon which was reversed by aspirin in muscle and WAT, in parallel with a reduction in JNK activity. In addition, our data show an impairment of insulin activation of IR and IRS-1 tyrosine phosphorylation in septic rats and, consistent with the reduction of IRS-1 serine phosphorylation observed in septic animals pretreated with aspirin, there was an increase in IRS-1 protein levels and tyrosine phosphorylation in muscle and WAT. Overall, these results provide important new insights into the mechanism of sepsis-induced insulin resistance.
ISSN:0006-291X
1090-2104
DOI:10.1016/j.bbrc.2004.06.048