LPL和Angptl4在糖尿病性心脏病发生发展中作用的研究新进展

发布时间：2018-03-10 14:54

本文选题：脂蛋白脂酶　切入点：血管生成素样蛋白　出处：《生理科学进展》2017年05期 　论文类型：期刊论文

【摘要】：糖尿病性心脏病是糖尿病的主要并发症,脂质代谢紊乱是糖尿病性心脏病发病机制之一。脂蛋白脂酶(lipoprotein lipase,LPL)是水解血浆中富含甘油三酯脂蛋白的关键酶。糖尿病早期,机体葡萄糖利用不足、糖耐量降低,LPL水解甘油三酯生成游离脂肪酸(free fatty acids,FFA)是心肌能量的主要来源。糖尿病中期,心肌细胞启动AMPK-p38MAPK/Hsp25-HPA-Notch信号通路进一步促进FFA生成为心肌供能。糖尿病晚期,过多FFA启动一系列机制诱导胰岛β细胞凋亡,使细胞内产生活性氧(reactive oxygen species,ROS)增多,通过促进缺氧诱导因子1α(hypoxia inducible factor1,HIF-1α)合成上调血管生成素样蛋白4(angiopoietin-like protein 4,Angptl4)表达,降低LPL活性,从而破坏心肌脂代谢稳态。本文主要综述LPL和Angptl4在糖尿病性心脏病发生发展中的可能作用。
[Abstract]:Diabetic heart disease is a major complication of diabetes, and lipid metabolism disorder is one of the pathogenesis of diabetic heart disease. Lipoprotein lipase lipase is a key enzyme in hydrolyzed plasma rich in triglyceride lipoprotein. LPL hydrolysis of triglycerides to produce free fatty acid free fatty acidsFFAs is the main source of myocardial energy. In the late stage of diabetes mellitus, excessive FFA initiated a series of mechanisms to induce the apoptosis of islet 尾 cells and increase the production of reactive oxygen species-ROSs in the cells. The expression of angiopoietin-like protein 4Angptl4) was upregulated by promoting the synthesis of hypoxia inducible factor-1 inducible factor-1 (HIF-1 伪) and the activity of LPL was decreased, thus destroying the homeostasis of myocardial lipid metabolism. The possible roles of LPL and Angptl4 in the occurrence and development of diabetic heart disease were reviewed in this paper.
【作者单位】：南华大学心血管疾病研究所动脉粥样硬化学湖南省重点实验室医学研究中心湖南省分子靶标新药研究协同创新中心;湖南省常德市第二人民医院科教科;
【基金】：国家自然科学基金(81270269,81370377) 湖南省南华大学基础医学重点学科建设项目资助课题
【分类号】：R541;R587.2

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