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首页> 外文期刊>Alcohol >Perspectives on alcohol consumption: liver polyunsaturated fatty acids and essential fatty acid metabolism.
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Perspectives on alcohol consumption: liver polyunsaturated fatty acids and essential fatty acid metabolism.

机译：饮酒的观点：肝脏多不饱和脂肪酸和必需脂肪酸的代谢。

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In this article, subjects diagnosed with alcoholic liver disease are shown to have lower concentrations of several polyunsaturated fatty acids (PUFAs), including 18:2n6, 18:3n6, 20:3n6, 18:3n3, 22:5n3, and 22:6n3, but not 20:4n6 and 22:4n6, nor 22:5n6, in the total lipid extracts of their livers compared with findings for specimens obtained from patients diagnosed with primary biliary cirrhosis and from control subjects. Findings of studies in animals have demonstrated that prolonged alcohol consumption reduces liver polyunsaturate content. However, the effect of ethanol on the elongation/desaturation of essential fatty acids is complex, as in vitro study results indicate that the direction of the effect of alcohol may be related to the dose of alcohol. Findings of studies in hepatocyte cell culture indicate that ethanol increased delta-5 and delta-6 desaturase activities throughout a broad concentration range. In contrast, lower liver desaturase activity has been reported in animals consuming high concentrations of alcohol (36%-40% energy) over a period of several months. Findings from in vivo isotope tracers studies in nonhuman primates and felines indicate that prolonged periods of moderate (mean consumption 2.6 g kg(-1) d(-1) and 1.2 g kg(-1) d(-1), respectively) alcohol consumption had no effect on the uptake of either linoleic (18:2n6) or alpha-linolenic (18:3n3) acids into the plasma and lead to an increased incorporation of these deuterated precursors into 20:4n6 and 22:6n3. Thus, this likely reflects a stimulated, rather than an inhibited, production of long-chain PUFAs. In numerous studies in various species, investigators have documented that alcohol consumption can increase the level of lipid peroxidation in tissues, and sustained periods of ethanol-induced peroxidation can deplete tissues of PUFAs. A hypothesis to rationalize the long-term effects of alcohol consumption on liver PUFA concentration that takes into consideration the effect of ethanol on essential fatty acid metabolism is presented.
机译：在本文中，被诊断患有酒精性肝病的受试者显示出较低的几种多不饱和脂肪酸（PUFA）浓度，包括18：2n6、18：3n6、20：3n6、18：3n3、22：5n3和22：6n3与从诊断为原发性胆汁性肝硬化的患者和对照组获得的标本相比，他们的肝脏总脂质提取物中没有发现20：4n6和22：4n6，也没有22：5n6。动物研究的结果表明，长期饮酒会降低肝脏多不饱和物的含量。然而，乙醇对必需脂肪酸的伸长/去饱和的影响是复杂的，因为体外研究结果表明，醇作用的方向可能与醇的剂量有关。肝细胞培养研究的结果表明，乙醇在很宽的浓度范围内都能增加delta-5和delta-6去饱和酶的活性。相比之下，据报道在几个月内消耗高浓度酒精（36％-40％能量）的动物体内肝脏去饱和酶活性较低。在非人类灵长类动物和猫科动物体内进行的同位素示踪研究的结果表明，中度酒精（分别平均消耗2.6 g kg（-1）d（-1）和1.2 g kg（-1）d（-1）的酒精的时间延长摄入对血浆中亚油酸（18：2n6）或α-亚麻酸（18：3n3）的摄取没有影响，并导致这些氘代前体在20：4n6和22：6n3中的掺入增加。因此，这可能反映了长链PUFA的受激产生而不是受抑制。在各种物种的众多研究中，研究人员已证明，饮酒可增加组织中脂质过氧化的水平，持续不断的乙醇诱导的过氧化可耗尽PUFAs的组织。提出了一个假设，以合理考虑酒精摄入对肝脏PUFA浓度的长期影响，其中考虑了乙醇对必需脂肪酸代谢的影响。

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