Perspectives on alcohol consumption: liver polyunsaturated fatty acids and essential fatty acid metabolism.
Perspectives on alcohol consumption: liver polyunsaturated fatty acids and essential fatty acid metabolism.
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饮酒的观点：肝脏多不饱和脂肪酸和必需脂肪酸代谢。
DOI：
10.1016/j.alcohol.2004.07.009
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发表时间：
2004
期刊：
影响因子：
--
通讯作者：
SalemJr,Norman
中科院分区：
文献类型：
--
作者：
Pawlosky,RobertJ;SalemJr,Norman
在本文中，诊断患有酒精性肝病的受试者肝脏总脂质提取物中多种多不饱和脂肪酸 (PUFA) 的浓度较低，包括 18:2n6、18:3n6、20:3n6、18:3n3、22:5n3 和 22:6n3，但不包括 20:4n6 和 22:4n6，也不包括 22:5n6与标本的结果进行比较 从诊断为原发性胆汁性肝硬化的患者和对照受试者中获得。动物研究结果表明，长期饮酒会降低肝脏多不饱和脂肪酸的含量。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，酒精作用的方向可能与酒精的剂量有关。肝细胞培养研究结果表明，乙醇在较宽的浓度范围内增加了 delta-5 和 delta-6 去饱和酶活性。相比之下，据报道，在几个月内消耗高浓度酒精（36%–40% 能量）的动物中，肝脏去饱和酶活性较低。非人灵长类动物和猫科动物体内同位素示踪剂研究的结果表明，长期适度饮酒（平均饮酒量分别为 2.6 g kg−1d−1 和 1.2 g kg−1d−1）对血浆中亚油酸 (18:2n6) 或 α-亚麻酸 (18:3n3) 的吸收没有影响，并导致掺入量增加 将这些氘代前体转化为 20:4n6 和 22:6n3。因此，这可能反映了长链 PUFA 的生产受到刺激，而不是受到抑制。在对不同物种的大量研究中，研究人员已经证明，饮酒会增加组织中脂质过氧化的水平，而持续的乙醇诱导的过氧化会消耗组织中的多不饱和脂肪酸。提出了合理化饮酒对肝脏 PUFA 浓度的长期影响的假设，该假设考虑了乙醇对必需脂肪酸代谢的影响。
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−1d−1and 1.2 g kg−1d−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.
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