摘要
本文比较了美国、欧洲和亚洲逐年增加的糖尿病患病率的估测报告，以警示人们更多地关注这一超出人们预测的事实。此外，还从几个方面对2型糖尿病的发病机制做了论述。内质网应激激活一系列的信号转导途径即未折叠蛋白反应（UPR），如果内质网应激不能缓解，UPR信号转导可促使凋亡细胞死亡。另外还对脂肪酸诱导脂肪细胞线粒体解耦联，腹型肥胖诱发的低水平炎性反应，来自血管周围脂肪的血管分泌信号转导和肌肉收缩引起的CaMK—MAPK—PGC一1线粒体生物合成等机制作了简要介绍。胰高血糖素样肽一1能调节胰岛B细胞的新生和增殖。c肽在单核细胞、巨噬细胞和CD4淋巴细胞趋化和动脉粥样硬化斑块的形成中都起重要的作用。胰岛素抵抗一直被视为糖尿病病因的中心，但随着体力活动减少和过度营养增加，腹型肥胖在胰岛素抵抗和其他糖尿病相关疾病发生中的作用逐渐显现。实际上，腹型肥胖，而不是胰岛素抵抗，为2型糖尿病的发病基础。
This review is to compare the increasing diabetes prevalence reported in USA, most European countries and Asia. The aim is to shock the people to pay much more attention to the increasing prevalence of diabetes beyond estimation. In addition, the mechanisms of type 2 diabetes are reviewed. Endoplasmic reticulum （ER） stress activates a set of signaling pathways, collectively termed the unfolded protein response （UPR）. UPR signaling can promote apoptotic cell death if ER stress is not alleviated. Fatty acid-induced mitochondria uncoupling in adipocytes, visceral obesity-induced low level inflammation, vasocrine signaling from perivascular fat and muscle contraction induced CaMK-MAPK-PGC-1-mitochondria biogenesis are described. GLP-1 can regulate the neogenesis and proliferation of islet β cell. C peptide plays a key role in the chemotaxis of monocyte, macrophage and CD4 lymphocyte, and the development of atherosclerosis. Insulin resistance has been the center of the pathogenesis of diabetes, but the role of visceral obesity in the development of insulin resistance, and of other diabetes-related disorders, is underscored by the rising trend of physical inactivity and overnutrition. Actually, visceral obesity, instead of the insulin resistance, often lays the foundation for the development of type 2 diabetes.
出处
《国际内分泌代谢杂志》
2008年第1期1-7,共7页
International Journal of Endocrinology and Metabolism
关键词
糖尿病
内质网应激
线粒体
腹型肥胖
炎症
胰岛素抵抗
Diabetes mellitus
Endoplasmic reticulum stress
Mitochondria
Visceral obesity
Inflammation
Insulin resistance.
