Insulin acutely upregulates protein expression of the fatty acid transporter CD36 in human skeletal muscle in vivo
Date
2008
Authors
Corpeleijn, E.
Pelsers, M.
Soenen, S.
Mensink, M.
Bouwman, F.
Kooi, M.
Saris, W.
Glatz, J.
Blaak, E.
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Journal article
Citation
Journal of Physiology and Pharmacology, 2008; 59(1):77-83
Statement of Responsibility
E. Corpeleijn, M. M.A.L. Pelsers, S. Soenen, M. Mensink, F. G. Bouwman, M. E. Kooi, W. H.M. Saris, J. F.C. Glatz, E. E. Blaak
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Abstract
Enhanced fatty acid uptake may lead to the accumulation of lipid intermediates. This is related to insulin resistance and type 2 diabetes mellitus. Rodent studies suggest that fatty acid transporters are acutely regulated by insulin. We investigated differences in fatty acid transporter content before and at the end of a hyperinsulinemic euglycemic clamp in skeletal muscle (m. vastus lateralis) of obese, glucose-intolerant men (IGT) and obese normal glucose tolerant controls (NGT). The fatty acid transporter FAT/CD36 protein content increased 1.5-fold (P < 0.05) after 3-hrs of insulin stimulation with no difference between IGT and control subjects. No change was seen in cytosolic fatty acid binding protein (FABPc) protein content. The increase in FAT/CD36 protein content was positively related to insulin resistance as measured during the clamp (r = 0.56, P < 0.05). An increase in FAT/CD36 protein content in skeletal muscle may result in a higher fractional extraction of fatty acids (larger relative uptake) after a meal, enhancing triglyceride accumulation in the muscle. We conclude that also in obese humans the FAT/CD36 protein content in skeletal muscle is dynamically regulated by insulin in vivo on the short term.
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