Effect of alcohol on lipoprotein metabolism. II. Lipolytic activities and mixed function oxidases.

Enzyme Pub Date : 1990-01-01 DOI:10.1159/000468704
J G Parkes, W Auerbach, D M Goldberg
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引用次数: 21

Abstract

The mechanism by which alcohol increases plasma total high density lipoproteins (HDLs) and HDL-cholesterol is unknown, but it may involve modulation of the lipolytic enzymes, hepatic triglyceride lipase (HTGL) and/or lipoprotein lipase (LPL) in hepatic and extrahepatic tissues. The modulation of HDL metabolism by alcohol may also be related to its potential to induce mixed function oxidases in liver microsomes. These possibilities were examined by a pair-feeding protocol in which rats were fed diets with 35% of the caloric content as ethanol; control groups received a diet with an isocaloric amount of sucrose or were fed chow ad libitum. Alcohol caused a significant decrease in HTGL activity of liver microsomes, but there was no significant effect of alcohol upon the activities of LPL in adipose tissue and heart muscle. The relative rates of mixed function oxidases, assayed in control liver microsomes using ethoxy-,pentoxy- and benzyloxy-resorufin as substrates, were benzyloxy greater than ethoxy greater than pentoxy. This order was not affected by alcohol, but the oxidation of ethoxy- and pentoxyresorufin was reduced in liver microsomes from the ethanol-fed group. HTGL synthesis and secretion were also measured using primary rat hepatocyte cultures isolated from animals on the above dietary regimes and maintained for up to 3 days in basal medium alone or supplemented with 10 mmol/l ethanol. In basal media the order of activity of extracellular HTGL, released by the addition of heparin, was sucrose-fed greater than chow-fed greater than ethanol-fed. The rate of HTGL secretion from hepatocytes was stimulated in ethanol-containing medium, and was greater in hepatocytes from the sucrose-fed controls.(ABSTRACT TRUNCATED AT 250 WORDS)

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酒精对脂蛋白代谢的影响。2脂溶活性和混合功能氧化酶。
酒精增加血浆总高密度脂蛋白(hdl)和高密度脂蛋白胆固醇的机制尚不清楚,但它可能涉及肝脏和肝外组织中脂溶酶、肝甘油三酯脂肪酶(HTGL)和/或脂蛋白脂肪酶(LPL)的调节。酒精对高密度脂蛋白代谢的调节也可能与它在肝微粒体中诱导混合功能氧化酶的潜力有关。这些可能性通过配对喂养方案进行了检验,在该方案中,大鼠的饮食中含有35%的卡路里含量为乙醇;对照组饲喂等量蔗糖或随意饲料。酒精使肝微粒体HTGL活性显著降低,但对脂肪组织和心肌中LPL活性无显著影响。在对照肝微粒体中,以乙氧基、戊氧基和苯氧基再间苯甲醚为底物,测定混合功能氧化酶的相对比率,苯氧基大于乙氧基,戊氧基大于乙氧基。这一顺序不受酒精的影响,但乙醇喂养组的肝微粒体中乙氧基和己氧基间苯二酚的氧化减少。利用从上述饮食方案中分离的大鼠肝细胞原代培养物,在基础培养基中单独或添加10 mmol/l乙醇中维持3天,测量HTGL的合成和分泌。在基础培养基中,添加肝素释放的细胞外HTGL活性的强弱顺序依次为:蔗糖饲料大于鲜饲料,乙醇饲料大于无糖饲料。在含乙醇的培养基中,肝细胞HTGL的分泌率受到刺激,而蔗糖喂养的对照组肝细胞的HTGL分泌率更高。(摘要删节250字)
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Functional hepatocellular heterogeneity for the production of plasma proteins. Liver cell heterogeneity: functions of non-parenchymal cells. Hepatocyte heterogeneity in the metabolism of carbohydrates. Zonal liver cell heterogeneity. Hepatocyte heterogeneity in the metabolism of amino acids and ammonia.
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