Abstract
In this study, we demonstrate that pretreatment with aspirin inhibits GH-induced insulin resistance. GH was observed to lead to serine phosphorylation of IRS-1, a phenomenon which was reversed by aspirin in liver, muscle and WAT in parallel with a reduction in JNK activity. In addition, our data show an impairment of insulin activation in the IR/IRS/PI(3)kinase pathway and a reduction in IRS-1 protein levels in rats treated with GH, which was also reversed in the animals pretreated with aspirin. Overall, these results provide new insights into the mechanism of GH-induced insulin resistance.
Publication types
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Research Support, Non-U.S. Gov't
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Retracted Publication
MeSH terms
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Adipose Tissue / drug effects
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Adipose Tissue / metabolism
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Animals
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Aspirin / pharmacology*
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Growth Hormone / pharmacology*
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Insulin / pharmacology
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Insulin Receptor Substrate Proteins
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JNK Mitogen-Activated Protein Kinases / metabolism
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Liver / drug effects
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Liver / metabolism
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Male
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Muscles / drug effects
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Muscles / metabolism
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Phosphoproteins / metabolism*
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Phosphorylation / drug effects
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Phosphoserine / metabolism*
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Proto-Oncogene Proteins c-jun / metabolism
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Rats
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Rats, Wistar
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Receptor, Insulin / metabolism
Substances
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Insulin
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Insulin Receptor Substrate Proteins
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Irs1 protein, rat
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Phosphoproteins
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Proto-Oncogene Proteins c-jun
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Phosphoserine
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Growth Hormone
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Receptor, Insulin
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JNK Mitogen-Activated Protein Kinases
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Aspirin