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Department of Human Biology (E.C., W.H.M.S., E.E.B.), Nutrition and Toxicology Research Institute NUTRIM, Maastricht University, 6200 MD Maastricht, The Netherlands; Laboratory for Toxicology, Pathology and Genetics (E.H.J.M.J.), and Centre for Nutrition and Health (E.J.M.F.), National Institute for Public Health and the Environment, 3720 BA Bilthoven, The Netherlands; and Department of Anesthesiology (P.M.H.J.R.), University Hospital Maastricht, 6200 MD Maastricht, The Netherlands
Address all correspondence and requests for reprints to: E. Corpeleijn, M.Sc., Department of Human Biology, Faculty of Health Sciences, Maastricht University, P.O. Box 616, 6200 MD Maastricht, The Netherlands. E-mail: E.Corpeleijn{at}hb.unimaas.nl.
Context: Obesity and type 2 diabetes mellitus are associated with increased levels of IL-6, a marker of inflammation.
Objective: This study addressed the question of whether IL-6 was released from skeletal muscle after a high-fat meal in men with impaired glucose tolerance (IGT), a prediabetic state, and whether IL-6 release could be reduced by weight loss.
Design: Skeletal muscle metabolism was studied in men with IGT (n = 11) and compared with men with normal glucose tolerance (NGT, n = 9), matched for body mass index and age. IL-6 flux over skeletal muscle was measured with the forearm model. Eight IGT men were willing to participate in a 12-wk weight loss program and were tested again.
Results: IL-6, but not C-reactive protein or TNF-
receptor 1 and 2, was released by skeletal muscle. Muscle IL-6 release was higher in IGT than in NGT during fasting (IGT = 2.26 ± 1.89 vs. NGT = 0.87 ± 0.48 fmol*100 ml tissue1*min1, P = 0.04) and after a meal (mean area under the curve per minute: IGT = 3.48 ± 2.63 vs. NGT = 1.37 ± 0.75 fmol*100 ml tissue1*min1; P = 0.03). In the IGT men, body weight loss resulted in a decrease of postprandial IL-6 release from skeletal muscle (52%; P = 0.04), reaching levels of the obese, NGT controls.
Conclusion: The present data suggest that a high-fat meal can evoke IL-6 release from muscle and that the IL-6 release is a consequence rather than a cause of the obese, insulin-resistant, and/or IGT state.
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H. Sell, K. Eckardt, A. Taube, D. Tews, M. Gurgui, G. Van Echten-Deckert, and J. Eckel Skeletal muscle insulin resistance induced by adipocyte-conditioned medium: underlying mechanisms and reversibility Am J Physiol Endocrinol Metab, June 1, 2008; 294(6): E1070 - E1077. [Abstract] [Full Text] [PDF] |
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