摘要
肥胖和胰岛素抵抗呈现一种慢性炎性反应状态，表现为白细胞介素-6、白细胞介素-1β、巨噬细胞趋化因子等炎性反应因子水平升高。其原因在于能量代谢不平衡导致脂肪细胞肥大、增生、内质网应激和线粒体功能障碍，c-Jun氨基末端激酶（JNK）／激活蛋白（AP）-1和核因子（NF）-κB抑制蛋白激酶（IKK）β／NF—κB两条信号通路活化，脂肪因子、游离脂肪酸和其他炎性反应介质表达增高，进而影响了全身各器官如肝脏、胰岛β细胞和骨骼肌。单核细胞和巨噬细胞是炎性反应因子另一个重要的来源。肥胖导致的JNK活化通过胰岛素受体底物-1的丝氨酸磷酸化影响胰岛素信号转导。饮食、运动、降低体重和药物可以改变炎性反应因子的水平。炎性反应理论为代谢性疾病的临床干预提供了重要的方向。
Obesity and insulin resistance are characterized by increased expression of markers and mediators of inflammation,which includes interleukin-6 （ IL-6 ） , interleukin-1β（IL-1β） , macrophage che- moattractant protein-1 （MCP-1）, etc. Chronic energy imbalance causes adipocyte hypertrophy and hyperplasia, endoplasmic reticulum stress, and mitochondrial dysfunction. These stress induced JNK/AP-1 and IKKβ/ NF-κB activation which lead to increased intracellular and systemic release of adipokines, free fatty acids, and inflammatory mediators that cause adipocyte dysfunction and induce adverse effects in the liver, pancreatic β-cells and skeletal muscle. Immune cells such as monocytes and macrophages are another source of inflammatory factors. Obesity-induced JNK activation promotes the phosphorylation of IRS-1 at serine sites. Diet, exercise, smoking and certain drugs are also associated with different levels of inflammatory markers. The evolving concept of inflammation provides new opportunities for using anti-inflammatory strategies to correct the metabolic disorders.
出处
《国际内分泌代谢杂志》
2008年第6期410-412,共3页
International Journal of Endocrinology and Metabolism
关键词
炎症
肥胖
胰岛素抵抗
巨噬细胞
Inflammation
Obesity
Insulin resistance
Macrophage
