Schwedhelm Carolina, Nimptsch Katharina, Bub Achim, Pischon Tobias, Linseisen Jakob
1Molecular Epidemiology Research Group,Max-Delbrück Center for Molecular Medicine in the Helmholtz Association,Robert-Rössle-Straße 10,13125 Berlin,Germany.
3Department of Physiology and Biochemistry of Nutrition,Max Rubner-Institut,Federal Research Institute of Nutrition and Food,Haid-und-Neu-Strasse 9,76131 Karlsruhe,Germany.
Br J Nutr. 2016 Feb 28;115(4):730-6. doi: 10.1017/S0007114515004985. Epub 2016 Jan 15.
High alcohol consumption is an important risk factor for chronic disease and liver degeneration. Paraoxonase (PON1) and arylesterase (AE) are functions of the enzyme paraoxonase, which is synthesised by the liver. Paraoxonase circulates in plasma bound to HDL and hydrolyses lipid peroxides, protecting lipoproteins against oxidative modification. It has been shown that excessive alcohol consumption leads to a reduction of serum PON1 and AE activities; however, studies investigating the association with low and moderate alcohol consumption are scarce. We investigated the cross-sectional association between alcohol consumption and serum activities of PON1 and AE using data from the population-based Bavarian Food Consumption Survey II survey. PON1 and AE activities were quantified in serum samples of 566 male and female study participants (aged 18-80 years), and dietary intake including alcohol consumption was estimated from three 24-h dietary recalls. The association between alcohol consumption and PON1 and AE activities was analysed using linear regression, adjusted for age, sex and socio-economic status. There was no strong association between alcohol consumption and enzymatic activities of PON1 and AE in the Bavarian population. PON1 activity was seen to be lowest in non-drinkers (0 g/d) and highest in people who consumed 15·1-30 g of alcohol/d. AE activity increased across alcohol consumption categories, with a mean maximum difference of 14 U/ml (P for linear trend 0·04). These associations were attenuated after adjustment for blood concentrations of HDL. The results of this study do not support the hypothesis that alcohol consumption is related to important alterations in PON1 and AE activities.
高酒精摄入量是慢性病和肝脏退化的重要风险因素。对氧磷酶（PON1）和芳基酯酶（AE）是由肝脏合成的对氧磷酶的功能。对氧磷酶在血浆中与高密度脂蛋白（HDL）结合循环，并水解脂质过氧化物，保护脂蛋白免受氧化修饰。研究表明，过量饮酒会导致血清PON1和AE活性降低；然而，关于低、中度饮酒与之关联的研究较少。我们利用基于人群的巴伐利亚食物消费调查II的数据，调查了饮酒与PON1和AE血清活性之间的横断面关联。对566名年龄在18 - 80岁的男性和女性研究参与者的血清样本中的PON1和AE活性进行了定量，并通过三次24小时饮食回忆估计了包括酒精摄入量在内的饮食摄入情况。使用线性回归分析饮酒与PON1和AE活性之间的关联，并对年龄、性别和社会经济地位进行了调整。在巴伐利亚人群中，饮酒与PON1和AE的酶活性之间没有强烈关联。PON1活性在不饮酒者（0克/天）中最低，在每天摄入15.1 - 30克酒精的人群中最高。AE活性在不同饮酒类别中增加，平均最大差异为14 U/ml（线性趋势P值为0.04）。在调整了HDL的血浓度后，这些关联减弱。本研究结果不支持饮酒与PON1和AE活性的重要改变有关这一假设。
