2型糖尿病
糖尿病
内分泌学
内科学
胰岛素抵抗
胰岛
胰岛素
载脂蛋白B
医学
葡萄糖稳态
糖耐量受损
平衡
小岛
胆固醇
作者
Lisa Juntti‐Berggren,Per‐Olof Berggren
出处
期刊:Current Opinion in Lipidology
[Ovid Technologies (Wolters Kluwer)]
日期:2017-02-01
卷期号:28 (1): 27-31
被引量:22
标识
DOI:10.1097/mol.0000000000000372
摘要
Purpose of review Type-1 and type-2 diabetes are diseases with an increasing number of patients and a complex, multifactorial pathogenesis. Apolipoprotein (apo) CIII is increased in both types of diabetes and interventions preventing the increase have effects on the development of diabetes. Recent findings ApoCIII affects intracellular Ca 2+ -handling by activating voltage-gated Ca 2+ -channels. ApoCIII is produced within the pancreatic islets and it increases in parallel with the development of insulin resistance and type-2 diabetes. Preventing the increase maintains a normal glucose tolerance as well as Ca 2+ -handling and no signs of inflammation can be seen in islets wherein the augmented local production of the apolipoprotein is absent. Summary ApoCIII has been found to interfere with both function and survival of the β-cell and thereby promote the development of diabetes. Increased levels of this apolipoprotein affects intracellular Ca 2+ -handling and insulin sensitivity, which finally results in impaired glucose homeostasis and diabetes. Interestingly, in a type-1 diabetes rat model lowering of apoCIII delays onset of diabetes. In type-2 diabetes insulin resistance within the pancreatic islets leads to a local increase in apoCIII that promotes inflammation and β-cell dysfunction. Hence, targeting apoCIII may constitute a novel pharmacological strategy to treat both type-1 and type-2 diabetes.
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