Abstract
Lifestyle interventions including exercise programmes are cornerstones in the prevention of obesity-related diabetes. In this study, we demonstrate that a single bout of exercise inhibits high-fat diet-induced insulin resistance. Diet-induced obesity (DIO) increased the expression and activity of the protein tyrosine phosphatase 1B (PTP1B) and attenuated insulin signalling in gastrocnemius muscle of rats, a phenomenon which was reversed by a single session of exercise. In addition, DIO was observed to lead to serine phosphorylation of insulin receptor substrate 1 (IRS-1), which was also reversed by exercise in muscle in parallel with a reduction in c-Jun N-terminal kinase (JNK) activity. Thus, acute exercise increased the insulin sensitivity during high-fat feeding in obese rats. Overall, these results provide new insights into the mechanism by which exercise restores insulin sensitivity.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Dietary Fats / administration & dosage*
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Dose-Response Relationship, Drug
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I-kappa B Proteins / antagonists & inhibitors
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Insulin / metabolism
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Insulin Receptor Substrate Proteins
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Insulin Resistance*
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JNK Mitogen-Activated Protein Kinases / antagonists & inhibitors
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JNK Mitogen-Activated Protein Kinases / metabolism
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Male
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Muscle, Skeletal / metabolism
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Obesity / etiology
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Obesity / metabolism
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Obesity / physiopathology*
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Phosphoproteins / chemistry*
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Phosphoproteins / metabolism*
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Phosphorylation
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Physical Conditioning, Animal*
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Protein Tyrosine Phosphatase, Non-Receptor Type 1
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Protein Tyrosine Phosphatases / metabolism*
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Rats
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Rats, Wistar
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Recovery of Function
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Serine / metabolism
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Signal Transduction
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Swimming
Substances
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Dietary Fats
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I-kappa B Proteins
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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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Serine
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JNK Mitogen-Activated Protein Kinases
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Protein Tyrosine Phosphatase, Non-Receptor Type 1
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Protein Tyrosine Phosphatases
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Ptpn1 protein, rat