Physical inactivity affects skeletal muscle insulin signaling in a birth weight-dependent manner |
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| Institution: | 1. Steno Diabetes Center, Gentofte, Denmark;2. Department of Biomedical Sciences, University of Copenhagen;3. Center for Healthy Ageing, University of Copenhagen;4. Molecular Physiology Group, The August Krogh Centre, Department of Nutrition, Exercise and Sports, University of Copenhagen;5. Rigshospitalet, Department of Endocrinology, Denmark;1. University Hospital Sainte Marguerite, Marseille, France;2. Outcomes Research, Novosys Health, Flemington, NJ, USA;3. Diabetes-Metabolism Franchise, Sanofi-Aventis US, Bridgewater, NJ, USA;4. Diabetes-Metabolism Franchise, Sanofi, Paris, France;5. University of Verona Medical School and Azienda Ospedaliera Universitaria Integrata di Verona, Verona, Italy;6. Dr Negrin Hospital, Las Palmas University, Las Palmas, Spain;7. Department of Diabetology, Endocrinology and Nutrition, Assistance Publique Hôpitaux de Paris, Bichat Hospital, Paris, France;8. INSERM, Research Unit 872, Paris, France;9. University Paris Diderot, Sorbonne Paris Cité, UFR de Médecine, Paris, France;10. Dallas Diabetes and Endocrine Center at Medical City, Dallas, TX, USA;1. Department of Internal Medicine – Section on Nephrology, Wake Forest School of Medicine, Winston-Salem, NC, USA;2. Center for Genomics and Personalized Medicine Research, Wake Forest School of Medicine, Winston-Salem, NC, USA;3. Center for Diabetes Research, Wake Forest School of Medicine, Winston-Salem, NC, USA;4. Department of Biochemistry, Wake Forest School of Medicine, Winston-Salem, NC, USA;5. Division of Public Health Sciences - Department of Biostatistical Sciences, Wake Forest School of Medicine, Winston-Salem, NC, USA;1. Laboratory for DNA Analysis and Molecular Diagnostics, Department of Nephrology, Medical University of Lublin, 20–954 Lublin, Poland;2. Department of Cardiology, Medical University of Lublin, 20–954 Lublin, Poland |
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| Abstract: | AimsWe investigated whether physical inactivity could unmask defects in insulin and AMPK signaling in low birth weight (LBW) subjects.MethodsTwenty LBW and 20 normal birth weight (NBW) subjects were investigated using the euglycemic–hyperinsulinemic clamp with excision of skeletal muscle biopsies pre and post 9 days of bed rest. Employing Western blotting, we investigated skeletal muscle Akt, AS160, GLUT4, and AMPK signaling.ResultsPeripheral insulin action was similar in the two groups and was decreased to the same extent post bed rest. Insulin and AMPK signaling was unaffected by bed rest in NBW individuals. LBW subjects showed decreased insulin-stimulated Akt phosphorylation and increased AMPK α1 and γ3 protein expression post bed rest. Insulin response of AS160 phosphorylation was lower in LBW subjects both pre and post bed rest.ConclusionsBed rest-induced insulin resistance is not explained by impaired muscle insulin or AMPK signaling in subjects with or without LBW. Lower muscle insulin signaling in LBW subjects post bed rest despite similar degree of insulin resistance as seen in controls may to some extent support the idea that LBW subjects are at higher risk of developing type 2 diabetes when being physically inactive. |
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