Increased insulin-stimulated Akt pSer and cytosolic SHP2 protein abundance in human skeletal muscle following acute exercise and short-term training
Journal of Applied Physiology, ISSN: 8750-7587, Vol: 102, Issue: 4, Page: 1624-1631
2007
- 25Citations
- 33Captures
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Metrics Details
- Citations25
- Citation Indexes25
- 25
- CrossRef18
- Captures33
- Readers33
- 33
Article Description
The purpose of the present study was to determine in human skeletal muscle whether a single exercise bout and 7 days of consecutive endurance (cycling) training 1) increased insulin-stimulated Akt pSer and 2) altered the abundance of the protein tyrosine phosphatases (PTPases), PTP1B and SHP2. In healthy, untrained men (n = 8; 24 ± 1 yr), glucose infusion rate during a hyperinsulinemic euglycemic clamp, when compared with untrained values, was not improved 24 h following a single 60-min bout of endurance cycling but was significantly increased (∼30%; P < 0.05) 24 h following completion of 7 days of exercise training. Insulin-stimulated Akt pSer was ∼50% higher (P < 0.05) 24 h following the acute bout of exercise, with this effect remaining after 7 days of training (P < 0.05). Insulin-stimulated insulin receptor and insulin receptor substrate-1 tyrosine phosphorylation were not altered 24 h after acute exercise and short-term training. Insulin did not acutely regulate the localization of the PTPases, PTP1B or SHP2, although cytosolic protein abundance of SHP2 was increased (P < 0.05; main effect) 24 h following acute exercise and short-term training. In conclusion, insulin-sensitive Akt pSer and cytosolic SHP2 protein abundance are higher after acute exercise and short-term training, and this effect appears largely due to the residual effects of the last bout of prior exercise. The significance of exercise-induced alterations in cytosolic SHP2 and insulin-stimulated Akt pSer on the improvement in insulin sensitivity requires further elucidation. Copyright © 2007 the American Physiological Society.
Bibliographic Details
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=34147134626&origin=inward; http://dx.doi.org/10.1152/japplphysiol.00821.2006; http://www.ncbi.nlm.nih.gov/pubmed/17185494; https://www.physiology.org/doi/10.1152/japplphysiol.00821.2006; http://jap.physiology.org/cgi/doi/10.1152/japplphysiol.00821.2006; http://jap.physiology.org/content/102/4/1624
American Physiological Society
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