抵抗素与肝脏胰岛素抵抗的关系

The relationship between resistin and hepatic insulin resistance

抵抗素是一种脂肪细胞因子,研究发现高抵抗素水平可诱导肝脏胰岛素抵抗发生,其机制可能是抑制腺苷酸活化蛋白激酶(AMPK)磷酸化,上调糖异生关键酶PEPCK和G6Pase的表达促进糖异生,从而使肝糖输出增多。肝脏是胰岛素作用的重要靶点,也是机体代谢的关键器官。肝脏胰岛素抵抗时,糖脂代谢紊乱加重机体胰岛素抵抗,促进2型糖尿病的发生。AMPK是物质代谢的关键激酶,通过磷酸化作用调节糖脂代谢相关酶的活性以及调节机体的能量平衡。抵抗素通过AMPK调节肝糖代谢这一观点为探讨抵抗素在胰岛素抵抗中的作用提供了新的思路。

As an adipocytokine, the relationship between resistin and insulin resistance remains unclear, The recent studies have shown that hyper-resistinemia induces insulin resistance. The potential mechanism is that resistin inhibits the phospborylation of AMP-activated protein kinase （AMPK） in the liver and upregulates the expressions of Glucose-6-phosphatase （G6Pase） and phosphoenolpyruvate carboxykinase （PEPCK）, which resuits in the elevation of gluconeogenesis and hepatic glucose output. Liver is the most important target for insulin action, as well as the center of metabolism. When hepatic insulin resistance happens, disorder of glucose and fatty acid metabolism aggravates the whole body insulin resistance, therefore hepatic insulin resistance may be the primary defect in the development of insulin resistance. AMPK is the key kinase of energy metabolism and regulates metabolic pathways in glucose and fatty acid metabolism and protein synthesis. The regulation of risistin in hepatic glucose metabolism is mediated by AMPK, which could lead to new insights into the role of resistin in insulin resistance.