CAJ | 학술논문

胰岛素抵抗是2型糖尿病(T2DM)主要病理生理机制之一.肝脏、肌肉和脂肪组织存在胰岛素抵抗.近年来研究显示,胰岛α细胞与β细胞也存在胰岛素抵抗.高糖、高游离脂肪酸(FFA)、氧化应激、炎性反应均可导致胰岛素抵抗:高糖作用可下调胰岛α、β细胞磷脂酰肌醇3激酶(PI3K)/蛋白激酶B(PKB)途径;高FFA抑制胰岛素受体底物(IRS)及PI3K活性;氧化应激使胰岛α、β细胞的IRS表达下降;炎性因子可干扰IRS/PI3K信号通路.
이도소저항시2형당뇨병(T2DM)주요병리생리궤제지일.간장、기육화지방조직존재이도소저항.근년래연구현시,이도α세포여β세포야존재이도소저항.고당、고유리지방산(FFA)、양화응격、염성반응균가도치이도소저항:고당작용가하조이도α、β세포린지선기순3격매(PI3K)/단백격매B(PKB)도경;고FFA억제이도소수체저물(IRS)급PI3K활성;양화응격사이도α、β세포적IRS표체하강;염성인자가간우IRS/PI3K신호통로.
Insulin resistance (IR) is one of the major pathogenesis of type 2 diabetes mellitus (T2DM).It existed in the liver,muscle and adipose tissue.Recent studies have shown that IR existed in α and β cells of pancreatic islets.Hyperglycemia,high free fatty acid ( FFA),oxidative stress and inflammatory response may lead to IR.Hyperglycemia reduced phosphatidylinositol 3-kinase (PI3K)/protein kinase B (PKB) channels in α and β cells of pancreatic islets.High FFA suppressed the activity of insulin receptor substrate (IRS) and PI3K.Oxidative stress reduced the expression of insulin receptor substrate in α and β cells of islets.Inflammatory factors interfered IRS/PI3Ksignaling pathways.