2型糖尿病生理病理到临床早期治疗方案的优化演示幻灯片.pptVIP

胰岛素介导的葡萄糖摄取 mean平均血浆胰岛素 胰岛素介导的葡萄糖摄取 mean平均血浆胰岛素compensatory hypersecretion补偿性分泌过多 The Starling curve of the pancreas 胰岛素介导的葡萄糖摄取 mean平均血浆胰岛素 胰岛素介导的葡萄糖摄取 mean平均血浆胰岛素 Change from baseline Caloric intake pathogenesis of Insulin Resistance Mitochondrial Dysfunction胰岛素抵抗发病机制的线粒体功能障碍 Acquired （aging） or inherited （IR offspring）defect of mitochondrial metabolism后天（老化）或继承IR后代）的线粒体代谢缺陷 在组织水平，胰岛素抵抗导致的结果包括肝脏、脂肪组织和肌肉中胰岛素依赖性葡萄糖摄入降低。 肝脏过量葡萄糖的生成，导致了高血糖。 另外，脂肪组织甘油三酯的过量的分解，导致了循环游离脂肪酸的浓度增加。而更为重要的，不仅在代谢过程中游离脂肪酸与葡萄糖的代谢相互竞争，而且不断增加的证据也证实了升高的游离脂肪酸对胰腺有毒性。 The consequences of insulin resistance at the tissue level include decreased insulin-dependent glucose uptake into liver, adipose tissue and muscle. This, combined with excessive glucose production by the liver, leads to hyperglycemia. In addition, excessive breakdown of triglycerides in the adipose tissue leads to increased circulating free fatty acids. This is particularly important since not only do free fatty acids compete for glucose during metabolism, but there is also increasing evidence that elevated free fatty acids are toxic to the pancreas. Fig 1 Declining ? cell function combines with increasing insulin resistance to produce non-insulin dependent diabetes. When insulin resistance is severe only a small fall in ? cell function is required to produce diabetes (thick lines). Conversely, in insulin sensitive subjects (such as native Japanese) a more severe fall in ? cell function is required (thin lines)  onset A reduction in HbA1c is associated with a reduction in complications * * Between-group differences in glycated haemoglobin levels were lost within 1 year after cessation of the randomly assigned treatments1, and such differences in blood-pressure levels were lost within 2 years after cessation2. However, levels of glycated haemoglobin continued to fall in both glucose-control groups1 and blood-pressure levels continued to fall in both blood-pressure groups2 during the first 5 years of post-trial monitoring (le