Lecomte E, Herbeth B, Paille F, Steinmetz J, Artur Y, Siest G
Laboratoire du Centre de Médecine Pr'eventive, Vandoeuvre-lés-Nancy, France.
Clin Chem. 1996 Oct;42(10):1666-75.
The effects of alcohol consumption on serum concentrations of apolipoproteins (apo) A-I, C-III, B, and E and of lipoproteins (Lp) A-I, A-I:A-II, C-III, C-III:B, and (a) were studied in 132 healthy subjects, including 55 low drinkers of alcohol (<20 g/day), 36 moderate drinkers (20-50 g/day), and 41 heavy drinkers (>50 g/day), and in 97 hospitalized alcoholic patients (> 100 g/day) without severe liver disease (especially functional insufficiency), before and after 21 days of withdrawal treatment. Serum concentrations of apo A-I, LpA-I, LpA-I:A-II, apo C-III, and LpC-III significantly (P </= 0.01) increased with alcohol intake (mean +/- SE in low drinkers vs in alcoholics)--1.45 +/- 0.03 vs 1.78 +/- 0.05 g/L; 0.45 +/- 0.02 vs 0.56 +/- 0.02 g/L; 0.99 +/- 0.02 vs 1.22 +/- 0.04 g/L; 27.6 +/- 1.5 vs 39.7 +/- 1.7 mg/L; and 8.4 +/- 0.9 vs 24.7 +/- 1.7 mg/L, respectively-whereas apo B and LpC-III:B concentrations tended to decrease--1.20 +/- 0.04 vs 1.06 +/- 0.04 g/L and 19.3 +/- 1.2 vs 14.9 +/- 1.0 mg/L, respectively. No significant difference between these four types of alcohol consumption was noticed for cholesterol, triglycerides, apo E, and Lp(a). After withdrawal, the concentrations of serum apo A-I, apo C-III, LpA-I, LpA-I:A-II, and LpC-III decreased significantly (P </= 0.01), reaching values comparable with those in low drinkers; concentrations of triglycerides, apo B, apo E, and Lp(a) rose; and cholesterol concentration was unaffected. In multiple regression analysis, after adjustment for serum concentrations of albumin, aspartate aminotransferase, and gamma-glutamyltransferase and for the Quetelet index, alcohol consumption remained positively correlated to apo A-I, LpA-I:A-II, apo C-III, and LpC-III concentrations. Study of other determinants of serum apo and lipoprotein concentrations suggests that alcohol-related variations in some of them, especially apo A-I, might depend on the metabolic ability of the liver to synthesize proteins and on induction phenomena. Finally, although the increase of antiatherogenic apo- and lipoproteins and the decrease of those known to be atherogenic were generally marked in alcoholics, alcohol-related modifications of these markers were very limited in our sample of French healthy men. We conclude, therefore, that moderate alcohol consumption (20-50 g/day) is unlikely to protect against ischemic heart disease through an effect on the proteins measured in this study.
在132名健康受试者（包括55名轻度饮酒者（<20克/天）、36名中度饮酒者（20 - 50克/天）和41名重度饮酒者（>50克/天））以及97名无严重肝脏疾病（尤其是功能不全）的住院酒精性肝病患者（>100克/天）中，研究了饮酒对血清载脂蛋白（apo）A - I、C - III、B和E以及脂蛋白（Lp）A - I、A - I:A - II、C - III、C - III:B和（a）浓度的影响。在戒酒治疗21天前后进行检测。随着酒精摄入量增加，血清apo A - I、LpA - I、LpA - I:A - II、apo C - III和LpC - III浓度显著（P≤0.01）升高（轻度饮酒者与酒精性肝病患者的均值±标准误）——分别为1.45±0.03与1.78±0.05克/升；0.45±0.02与0.56±0.02克/升；0.99±0.02与1.22±0.04克/升；27.6±1.5与39.7±1.7毫克/升；以及8.4±0.9与24.7±1.7毫克/升，而apo B和LpC - III:B浓度则呈下降趋势——分别为1.20±0.04与1.06±0.04克/升以及19.3±1.2与14.9±1.0毫克/升。对于胆固醇、甘油三酯、apo E和Lp(a)，这四种饮酒类型之间未发现显著差异。戒酒之后，血清apo A - I、apo C - III、LpA - I、LpA - I:A - II和LpC - III浓度显著下降（P≤0.01），降至与轻度饮酒者相当的值；甘油三酯、apo B、apo E和Lp(a)浓度上升；胆固醇浓度未受影响。在多元回归分析中，在对血清白蛋白、天冬氨酸转氨酶和γ - 谷氨酰转移酶浓度以及体重指数进行校正之后，饮酒量仍与apo A - I、LpA - I:A - II、apo C - III和LpC - III浓度呈正相关。对血清apo和脂蛋白浓度的其他决定因素的研究表明，其中一些因素（尤其是apo A - I）与酒精相关的变化可能取决于肝脏合成蛋白质的代谢能力以及诱导现象。最后，尽管酒精性肝病患者中抗动脉粥样硬化的apo和脂蛋白增加以及已知致动脉粥样硬化的成分减少的情况通常较为明显，但在我们的法国健康男性样本中，这些标志物与酒精相关的变化非常有限。因此，我们得出结论，中度饮酒（20 - 50克/天）不太可能通过对本研究中所测蛋白质的影响来预防缺血性心脏病。
