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机构地区:[1]泰山医学院动脉粥样硬化研究所,山东省高校动脉粥样硬化重点实验室,泰安271000
出 处:《生物化学与生物物理进展》2015年第9期804-809,共6页Progress In Biochemistry and Biophysics
基 金:国家自然科学基金(81170785);山东省泰山学者工程专项基金(200867)资助项目~~
摘 要:高密度脂蛋白(HDL)保护血管的主要活性成分载脂蛋白AⅠ和磷酸鞘氨醇1的细胞表面受体皆存在于脂肪组织,而参与HDL重构的脂质转运蛋白亦在脂肪组织高表达,提示HDL可以通过上述成分调节脂肪细胞能量代谢.相关分子机制研究发现,健康人体内和重组的HDL颗粒皆可活化脂肪细胞腺苷酸激活蛋白激酶(AMPK),并抑制脂肪酸氧化,而体外和体内实验均证明HDL可能通过其主要活性成分的多个受体途径协调激活AMPK活性,从而参与调节脂肪细胞能量代谢.期待HDL对脂肪细胞AMPK的调节作用研究能为防治脂肪代谢异常所致肥胖性疾患提供新的治疗靶点.The receptors of apolipoprotein A I and sphingosine 1-phosphate, two main factors mediating the protective effects of high-density lipoprotein (HDL) on blood vessels, are located in adipose tissues. Also, the lipid transfer proteins which mediate HDL remodeling are highly expressed in adipose tissues, suggesting HDL may regulate adipocyte energy metabolism through its components. It is known HDL particles isolated from healthy subjects or recombinant HDLs activate AMP-activated protein kinase (AMPK) in adipocytes and inhibit the oxidation of fatty acids. Further, in vitro and in vivo experiments confirm that the active components in HDL may activate AMPK activity by their receptor pathway, which may contribute to the regulating effects of HDL on adipocyte energy metabolism. It will be expected that studies in the effect of HDL on adipocyte AMPK may provide a new therapeutic target for prevention and treatment of obesity caused by abnormal fat metabolism.
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