Guiraud Annabelle, de Lorgeril Michel, Zeghichi Sabrina, Laporte François, Salen Patricia, Saks Valdur, Berraud Nathalie, Boucher François, de Leiris Joël
TIMC-IMAG, CNRS UMR 5525, Laboratoire PRETA Coeur et Nutrition, Faculté de Médecine, Université Joseph Fourier, Grenoble, France.
Br J Nutr. 2008 Dec;100(6):1237-44. doi: 10.1017/S0007114508981472. Epub 2008 Apr 29.
Moderate ethanol drinking (ED) and n-3 fatty acids have both been associated with low cardiac mortality. However, there are few data evaluating the interactions of ED with n-3. We recently reported that moderate ED results in increased n-3 in cardiac patients. The main aim of the present study was, through a well-controlled experimental model, to confirm that chronic ED actually results in increased n-3. Secondary aims were to examine the effects of chronic ED on cardiac mitochondria, cardiac function and experimental myocardial infarction. We studied the fatty acid profiles of plasma, cell membranes and cardiac mitochondria phospholipids in a rat model of chronic ED. In plasma and cell membranes, ED actually resulted in higher n-3 (P = 0.005). In mitochondria phospholipids of ED rats, n-3 were also increased (P < 0.05) but quite modestly. Cardiac mitochondrial function and left ventricular function were not significantly different in ED and control rats, while infarct size after 30 min ischaemia and reperfusion was smaller (P < 0.0001) in ED rats. This is the first animal study confirming interaction of alcohol drinking with n-3. We found no harmful effect of chronic ED on the heart in that model but a significant cardioprotection. Further studies are warranted to investigate the mechanisms by which moderate ED alters the metabolism of n-3 and whether n-3 are the mediators of the ED-induced cardioprotection.
适度饮酒（ED）和n-3脂肪酸均与较低的心脏死亡率相关。然而，评估ED与n-3相互作用的数据很少。我们最近报告称，适度饮酒会导致心脏病患者体内n-3增加。本研究的主要目的是通过一个严格控制的实验模型，证实长期饮酒确实会导致n-3增加。次要目的是研究长期饮酒对心脏线粒体、心脏功能和实验性心肌梗死的影响。我们在长期饮酒的大鼠模型中研究了血浆、细胞膜和心脏线粒体磷脂的脂肪酸谱。在血浆和细胞膜中，饮酒实际上导致了更高的n-3含量（P = 0.005）。在饮酒大鼠的线粒体磷脂中，n-3也有所增加（P < 0.05），但增幅相当小。饮酒大鼠和对照大鼠的心脏线粒体功能和左心室功能没有显著差异，而在30分钟缺血和再灌注后，饮酒大鼠的梗死面积较小（P < 0.0001）。这是第一项证实饮酒与n-3相互作用的动物研究。我们发现在该模型中，长期饮酒对心脏没有有害影响，反而有显著的心脏保护作用。有必要进行进一步的研究，以探讨适度饮酒改变n-3代谢的机制，以及n-3是否是饮酒诱导心脏保护作用的介质。
