Department of Cardiology, First Clinical College of Harbin Medical University, Harbin, China.
Med Sci Monit. 2011 Jan;17(1):BR1-9. doi: 10.12659/msm.881311.
Chronic alcohol intake exerts myocardial damage en route to the development of alcoholic cardiomyopathy (ACM), although the precise pathogenesis of ACM is unknown. Carnitine is known to participate in the regulation of metabolism in a number of heart diseases. This study was designed to examine the interplay between myocardial metabolism and carnitine in the development of ACM.
MATERIAL/METHODS: Experimental animals were divided into 3 groups: (i) group A: alcohol-fed. (ii) group B: alcohol/carnitine: (200mg/kg/d, p.o. by mixing carnitine in rat chow). (iii) group C: control. Blood levels of free fatty acid (FFA), total carnitine (TC) and free carnitine (FC) were monitored in rats receiving alcohol with or without carnitine. Mitochondrial adenine nucleotide translocator-1 (ANT1) activity, ATPase activity, high energy phosphate concentration, peroxisome proliferator-activated receptor-α (PPARα), carnitine-palmitoyl transferase I (CPT-I), medium-chain acyl-coenzyme A dehydrogenase (MCAD), ANT1 and ATPase mRNA and protein expression were also monitored in myocardial tissue.
Experimental animals received alcohol with or without carnitine for six 6 months. Our results indicated that FFA increased abruptly. TC and FC were significantly decreased in groups receiving alcohol at 4 months. The concentration of ATP, ADP and AMP in the myocardium decreased following 2 months of alcohol administration. mRNA and protein expression of PPARα, CPT-I, MCAD, ANT1 and ATPase expressions were gradually altered in groups following alcohol feeding.
These observations suggest that abnormal metabolism is present in the myocardium during the development of ACM. Carnitine may improve myocardial metabolism by elevating the content of PPARα, CPT-I and MCAD.
慢性酒精摄入会对心肌造成损伤，进而导致酒精性心肌病（ACM）的发生，尽管 ACM 的具体发病机制尚不清楚。肉碱已知参与多种心脏病的代谢调节。本研究旨在探讨心肌代谢与肉碱在 ACM 发生发展过程中的相互作用。
材料/方法：实验动物分为 3 组：（i）组 A：酒精喂养组。（ii）组 B：酒精/肉碱组（200mg/kg/d，通过将肉碱混入大鼠饲料中进行口服）。（iii）组 C：对照组。在给予酒精的同时或不给予肉碱的情况下监测接受酒精的大鼠的游离脂肪酸（FFA）、总肉碱（TC）和游离肉碱（FC）水平。监测心肌组织中线粒体腺嘌呤核苷酸转运体-1（ANT1）活性、ATP 酶活性、高能磷酸浓度、过氧化物酶体增殖物激活受体-α（PPARα）、肉碱棕榈酰转移酶 I（CPT-I）、中链酰基辅酶 A 脱氢酶（MCAD）、ANT1 和 ATP 酶 mRNA 和蛋白表达。
实验动物接受酒精加或不加肉碱喂养共 6 个月。我们的结果表明 FFA 急剧增加。接受酒精的两组在 4 个月时 TC 和 FC 显著降低。酒精给药 2 个月后，心肌中 ATP、ADP 和 AMP 的浓度降低。在接受酒精喂养的各组中，PPARα、CPT-I、MCAD、ANT1 和 ATP 酶的 mRNA 和蛋白表达逐渐改变。
这些观察结果表明，在 ACM 的发展过程中，心肌存在异常代谢。肉碱通过提高 PPARα、CPT-I 和 MCAD 的含量，可能改善心肌代谢。
