Sell Henrike, Dietze-Schroeder Daniela, Eckel Jürgen
Institute of Clinical Biochemistry and Pathobiochemistry, German Diabetes Center, Düsseldorf, Germany.
Trends Endocrinol Metab. 2006 Dec;17(10):416-22. doi: 10.1016/j.tem.2006.10.010. Epub 2006 Nov 3.
Insulin resistance in skeletal muscle is linked to an elevated adipose tissue mass, as is found in obesity, but can also be observed in lipodystrophy, in which adipose tissue is greatly reduced. Adipose tissue releases endocrine and metabolic mediators and is actively involved in crosstalk with skeletal muscle, a process that precedes and underlies the development of insulin resistance in muscles. Adipokines including tumor necrosis factor alpha, interleukin-6, leptin and adiponectin influence insulin signaling in skeletal muscle. Free fatty acids, their metabolites and ectopic fat in muscle also contribute to insulin resistance. Recent research indicates inflammation, endoplasmic reticulum stress and oxidative stress could be underlying mechanisms at the center of the development of insulin resistance. Insights into the role of macrophages in adipose tissue add to the complicated interplay between adipose tissue and skeletal muscle.
骨骼肌中的胰岛素抵抗与脂肪组织量增加有关,如在肥胖症中所见,但在脂肪营养不良中也可观察到,脂肪营养不良中脂肪组织大大减少。脂肪组织释放内分泌和代谢介质,并积极参与与骨骼肌的相互作用,这一过程先于肌肉中胰岛素抵抗的发展并是其基础。包括肿瘤坏死因子α、白细胞介素-6、瘦素和脂联素在内的脂肪因子会影响骨骼肌中的胰岛素信号传导。游离脂肪酸、其代谢产物以及肌肉中的异位脂肪也会导致胰岛素抵抗。最近的研究表明,炎症、内质网应激和氧化应激可能是胰岛素抵抗发展核心的潜在机制。对巨噬细胞在脂肪组织中作用的深入了解,进一步增加了脂肪组织与骨骼肌之间复杂的相互作用。