内科学
内分泌学
ABCG1公司
ABCA1
胆固醇
胰岛素
胆固醇逆向转运
2型糖尿病
胰岛素抵抗
糖尿病
生物
化学
脂蛋白
医学
生物化学
运输机
基因
作者
Arnold von Eckardstein,Rahel Sibler
出处
期刊:Current Opinion in Lipidology
[Ovid Technologies (Wolters Kluwer)]
日期:2010-11-23
卷期号:22 (1): 26-32
被引量:133
标识
DOI:10.1097/mol.0b013e3283412279
摘要
Purpose of review Low HDL cholesterol and hypertriglyceridemia as well as lowering of LDL cholesterol with statins increase the risk of T2DM. We discuss the recent findings on the effects of lipoproteins and cholesterol on the function and survival of pancreatic β-cells as well as on obesity and insulin sensitivity of muscle and liver. Recent findings LDL inhibits glucose-stimulated insulin secretion and proliferation of β-cells by LDL-receptor dependent and independent mechanisms, respectively. ApoA-I and HDL stimulate insulin secretion by interaction with ABCA1, ABCG1 or SR-BI and also inhibit apoptosis of β-cells. Mice with targeted knockouts of ABCA1 or ABCG1 in β-cells show reduced insulin secretion and glucose tolerance. ABCG1 contributes to the enrichment of insulin secretory granules with cholesterol, which is needed for their formation and trafficking to the plasma membrane whereas ABCA1-mediated cholesterol efflux from the plasma membrane appears to be important for their subsequent exocytosis. In mice, overexpression of apoA-I decreases body fat accumulation and increases insulin sensitivity of muscle and liver by inducing the phosphorylation of AMP kinase. Summary LDL, HDL and cholesterol regulate the function and survival of β-cells. HDL also exerts antiobesity and insulin-sensitizing effects. Thus dyslipidemias may not only be consequences but also contributors to the pathogenesis and hence targets for prevention of T2DM.
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