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β3肾上腺素受体介导的脂解作用与缺血性心衰的关系(PDF)

《心脏杂志》[ISSN:1009-7236/CN:61-1268/R]

期数:
2006年第6期
页码:
705-709
栏目:
综述
出版日期:
2006-12-25

文章信息/Info

Title:
β3-adrenergic receptormediated lipolysis and ischemic heart failure
作者:
潘红星; 谭学瑞
汕头大学医学院第一附属医院心内科，广东 汕头 515041
Author(s):
PAN Hong-Xing;  TAN Xue-Rui
Department of Cardiology, First Affiliated Hospital of Shantou University Medical College, Shantou ,Guangdong 515041,China
关键词:
β3肾上腺素受体; 脂解作用; 心力衰竭; 缺血性
Keywords:
β3-adrenergic receptor;  lipolysis;  heart failure; ischemic
分类号:
R541.6
DOI:
-
文献标识码:
A
摘要:
β3肾上腺素受体（β3AR）是新发现的受体，主要参与脂肪组织甘油三酯的降解，产生能量；心衰时心脏中β3AR上调；心肌缺血缺氧时，内源性脂解作用可维持心肌的收缩性；为了维持心功能慢性缺血性心衰代偿期很可能存在能量代谢重建：在神经内分泌激活的同时,以外源性游离脂肪酸（FFA）为主要能量底物，心脏缺血缺氧进一步加重时,β3AR代偿性上调并介导心肌细胞的内源性脂解供能，葡萄糖经由3磷酸甘油参与合成内源性三酰甘油再脂解而间接供能，葡萄糖的氧化被抑制，此时心肌细胞兼有类似脂肪细胞的功能。心衰时β3AR上调是能量代谢代偿的结果。但上调的β3-AR长期过度激活有可能引起心肌组织继发性肉碱缺乏，导致ATP生成障碍使心衰失代偿，因而在心衰失代偿期β3AR阻滞剂可能有利于缓解心衰。而(β3-AR激动药最终表现为正性肌力作用还是负性肌力作用，要看在具体的作用部位它对 β3AR的直接效应与其对胰岛素的继发效应二者的力量对比)。 从理论上讲，β3- AR激动药用于慢性缺血性心衰代偿期，既可改善心肌的能量代谢，产生正性肌力作用，又可降低动脉血压，降低心脏的前负荷，从而改善心功能；β3-AR激动药还可改善与心衰并存的胰岛素抵抗。心脏能量代谢的缺陷越来越被认为在心衰的进展中起着重要的决定性作用，心脏的代谢适应和适应不良是很有前景的药物治疗新靶点。
Abstract:
The newly-discovered β3adrenergic receptor (β3AR) is mainly involved in energy production via lipolysis in adipose tissue; the lipolysis of endogenous triacylglycerols in myocardium contributes to the maintenance of myocardial contractility. During the compensation of ischemic heart failure, there exists the efficient and enhanced energy metabolism shortcut: accompanying the activation of the nerveendocrine system, the failing heart utilizes exogenous free fatty acid as the predominant energy substrate ; while myocardial ischemia deteriorates further, the compensatorilyupregulated β3AR in myocardium mediates endogenous lipolysis to provide energy; glucose indirectly produces energy via its rapid shift to glycerol 3phosphate to form endogenous triacylglycerols; glucose oxidation is inhibited and myocardial cells concurrently function as the adipocytes. The upregulation of β3AR in failing heart may result from compensation of myocardial energy metabolism. But the constant activation of the upregulated β3AR may result in secondary carnitine insufficiency in myocardium. This contributes to reduced energy production and decompensated cardiac function. Therefore, β3AR antagonist can help improve cardiac function during decompensation. The ultimate inotropic effect of β3AR agonist depends on which one of its two effects, direct effect on β3AR or secondary effect on insulin, is advantaged at the specific action site in the body. Theoretically, during compensation, β3AR agonist strengthens cardiac function by ameliorating energy metabolism, causing positive inotropic effect and decreasing blood pressure which is the preload of the heart. Meanwhile, β3AR agonist can reduce the concomitant insulin resistance of the heart. Defects in energy metabolism are increasingly considered as a important determinant in the progression of heart failure. Promisingly, pharmacotherapy might be targeted at metabolic adaptation and maladaptation of the heart.

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备注/Memo

备注/Memo:
收稿日期：2006-03-07.supported by science and technology progran of Guangdong Province(No.2003C30613) Correspondence to：TAN Xue-rui Tel: 0754-8552841 Email:tanxuerui@vip.sina.com
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