Corpeleijn Eva, Saris Wim H M, Jansen Eugène H J M, Roekaerts Paul M H J, Feskens Edith J M, Blaak Ellen E
Department of Human Biology, Nutrition and Toxicology Research Institute, Maastricht University, P.O. Box 616, 6200 MD Maastricht, The Netherlands.
J Clin Endocrinol Metab. 2005 Oct;90(10):5819-24. doi: 10.1210/jc.2005-0668. Epub 2005 Jul 19.
Obesity and type 2 diabetes mellitus are associated with increased levels of IL-6, a marker of inflammation.
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.
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.
IL-6, but not C-reactive protein or TNF-alpha 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 x 100 ml tissue(-1) x min(-1), 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 x 100 ml tissue(-1) x min(-1); 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.
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.
肥胖和2型糖尿病与炎症标志物白细胞介素-6（IL-6）水平升高有关。
本研究探讨糖耐量受损（IGT，一种糖尿病前期状态）男性在高脂餐后骨骼肌是否释放IL-6，以及体重减轻是否能减少IL-6的释放。
对IGT男性（n = 11）的骨骼肌代谢进行研究，并与年龄和体重指数相匹配的糖耐量正常（NGT，n = 9）男性进行比较。采用前臂模型测量骨骼肌的IL-6通量。8名IGT男性愿意参加为期12周的体重减轻计划，并再次接受测试。
骨骼肌释放IL-6，但不释放C反应蛋白或肿瘤坏死因子-α受体1和2。空腹时，IGT组肌肉IL-6释放高于NGT组（IGT = 2.26 ± 1.89 vs. NGT = 0.87 ± 0.48 fmol×100 ml组织⁻¹×min⁻¹，P = 0.04），餐后也是如此（每分钟曲线下平均面积：IGT = 3.48 ± 2.63 vs. NGT = 1.37 ± 0.75 fmol×100 ml组织⁻¹×min⁻¹；P = 0.03）。在IGT男性中，体重减轻导致餐后骨骼肌IL-6释放减少（-52%；P = 0.04），达到肥胖的NGT对照组水平。
目前的数据表明，高脂餐可诱发肌肉释放IL-6，且IL-6释放是肥胖、胰岛素抵抗和/或IGT状态的结果而非原因。
