脂毒性
胰岛素抵抗
医学
内科学
内分泌学
糖尿病
2型糖尿病
辅酶Q10
发病机制
胰岛素
β细胞
胰岛素受体
2型糖尿病
过氧化物酶体增殖物激活受体γ
过氧化物酶体增殖物激活受体
生物信息学
受体
生物
小岛
作者
Michael Stümvoll,Barry J. Goldstein,Timon W. van Haeften
出处
期刊:The Lancet
[Elsevier]
日期:2005-04-01
卷期号:365 (9467): 1333-1346
被引量:2367
标识
DOI:10.1016/s0140-6736(05)61032-x
摘要
Type 2 diabetes mellitus has become an epidemic, and virtually no physician is without patients who have the disease. Whereas insulin insensitivity is an early phenomenon partly related to obesity, pancreas beta-cell function declines gradually over time already before the onset of clinical hyperglycaemia. Several mechanisms have been proposed, including increased non-esterified fatty acids, inflammatory cytokines, adipokines, and mitochondrial dysfunction for insulin resistance, and glucotoxicity, lipotoxicity, and amyloid formation for beta-cell dysfunction. Moreover, the disease has a strong genetic component, but only a handful of genes have been identified so far: genes for calpain 10, potassium inward-rectifier 6.2, peroxisome proliferator-activated receptor gamma, insulin receptor substrate-1, and others. Management includes not only diet and exercise, but also combinations of anti-hyperglycaemic drug treatment with lipid-lowering, antihypertensive, and anti platelet therapy.
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