2型糖尿病长期血糖干预研究.pptVIP

* The underlying factors that drive the pathogenesis of 2型糖尿病 are 胰岛素 抵抗 和 β-细胞 失功能. The triggers of the pathogenic process may include a genetic predisposition 或 environmental factors such as obesity – particularly abdominal obesity1 – 或 a sedentary lifestyle. 胰岛素 抵抗 decreases the effect of 胰岛素 in the tissues. This 降低胰岛素-dependent 葡萄糖 摄取 into muscle 和 adipose tissue 和 leads to excessive 葡萄糖 production by the liver. Consequently 高血糖develops, which is compensated for by an increase in 胰岛素 secretion. If there is a genetic 或 acquired defect in the ?-细胞, increased 胰岛素 secretion can no longer be maintained, causing 高血糖to reach 2型糖尿病 levels.2 Hence, development of 2型糖尿病 requires ?-细胞 失功能 on a background of 胰岛素 抵抗. Karter AJ, et al. 糖尿病 Obes Metab 2005;7:230–238. DeFronzo RA. 糖尿病 1988;37:667–687. * 磺脲类s (e.g. glyburide, glipizide, chlorpropamide) lower fasting 血糖 concentrations primarily by stimulating 胰岛素 secretion through interaction with potassium-sensitive ATP channels in the pancreatic β-细胞 membrane, resulting in calcium 摄取 和 胰岛素 release.1 Meglitinides (e.g. repaglinide) bind to ATP-sensitive potassium channels on pancreatic β-细胞s, increase 胰岛素 secretion, 和 reduce 血糖.1 二甲双胍 lowers 血糖 by inhibiting hepatic 葡萄糖 production 和 enhancing 胰岛素-stimulated 葡萄糖 transport in skeletal muscle.1 ?-glucosidase 抑制剂 (e.g. 阿卡波糖) slow the rate of carbohydrate digestion, thereby providing an alternative means to reduce postprandial 高血糖.1 DPP-4 抑制剂 (e.g. sitagliptin, vildagliptin) pr事件 the inactivation of glucagon-like peptide-1 (GLP?1). This increases circulating levels of active GLP-1, stimulates 胰岛素 secretion 和 inhibits glucagon secretion, resulting in lowering of 葡萄糖 levels.2 GLP-1 agonists (e.g. 艾塞那肽, liraglutide) mimic the action of GLP-1, a gut hormone released post-prandially, which stimulates 胰岛素 secretion and 胰岛素 gene expression as well as pancreatic β-细胞 growth.3 噻唑烷二酮类(e.g. 罗格列酮, 砒格列酮) decrease 胰岛素 抵抗 in fat, muscle and liver. In addition, they improve estimates