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首页> 外文期刊>Current opinion in lipidology >High density lipoproteins in the intersection of diabetes mellitus, inflammation and cardiovascular disease.
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High density lipoproteins in the intersection of diabetes mellitus, inflammation and cardiovascular disease.

机译：高密度脂蛋白在糖尿病，炎症和心血管疾病的交集中。

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PURPOSE OF REVIEW: Low HDL-cholesterol, diabetes mellitus and elevated C-reactive protein as well as various inflammatory diseases are risk factors for coronary heart disease. Both diabetes mellitus and inflammation decrease HDL-cholesterol. We summarize recent findings on the mechanisms underlying low HDL-cholesterol in diabetes and inflammation, as well as on novel functions of HDL that may protect not only from atherosclerosis but also from diabetes mellitus and inflammation-induced organ damage. RECENT FINDINGS: Elevated levels of non-esterified fatty acids and disturbed insulin action contribute to low HDL-cholesterol in diabetes mellitus by modifying lipolysis, apolipoprotein A-I production, as well as the activities of adenosine triphosphate-binding cassette transporter A1 and lipid transfer. Inflammation causes low HDL-cholesterol by increasing the activities of endothelial lipase and soluble phospholipase A2 and by replacing apolipoprotein A-I in HDL with serum amyloid A. HDL and lysosphingolipids therein have been identified as activators of the protein kinase Akt, which in turn is a regulator of apoptosis in beta-cells, endothelial cells, and smooth muscle cells, as well as a regulator of nitric oxide production and adhesion molecule expression in endothelial cells. SUMMARY: The protective properties of HDL in cytokine production, lipid oxidation, cholesterol efflux and reverse cholesterol transport make HDL a protective agent in inflammation-induced organ damage including diabetes mellitus. However, inflammation and diabetes cause a decrease in HDL-cholesterol concentrations and impair HDL function, placing HDL into the centre of a vicious cycle that may escalate into diabetes mellitus, inflammation-induced organ damage and atherosclerosis.
机译：审查目的：低HDL-胆固醇，糖尿病和C反应蛋白升高以及各种炎症性疾病是冠心病的危险因素。糖尿病和炎症都会降低HDL-胆固醇。我们总结了关于低水平的HDL-胆固醇在糖尿病和炎症中的潜在作用的最新发现，以及对HDL的新功能的发现，这些新功能不仅可以保护免受动脉粥样硬化的侵害，还可以保护糖尿病和炎症引起的器官损害。最近的发现：未酯化脂肪酸的水平升高和胰岛素作用受到干扰，可通过改变脂解作用，载脂蛋白A-1的产生以及三磷酸腺苷结合盒转运蛋白A1的活性和脂质转移来降低糖尿病患者的HDL-胆固醇。炎症通过增加内皮脂肪酶和可溶性磷脂酶A2的活性，并用血清淀粉样蛋白A代替HDL中的载脂蛋白AI，从而导致HDL-胆固醇降低。HDL和其中的鞘糖脂已被鉴定为蛋白激酶Akt的激活剂，而后者又是调节剂β细胞，内皮细胞和平滑肌细胞凋亡的调控，以及内皮细胞中一氧化氮生成和粘附分子表达的调节剂。摘要：HDL在细胞因子产生，脂质氧化，胆固醇外排和反向胆固醇转运中的保护特性使HDL在炎症引起的器官损害（包括糖尿病）中成为保护剂。但是，炎症和糖尿病会导致HDL-胆固醇浓度降低并损害HDL功能，使HDL进入恶性循环的中心，恶性循环可能会升级为糖尿病，炎症引起的器官损害和动脉粥样硬化。

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