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首页> 外文期刊>The Internet Journal of Pharmacology >Glycine Modulates Lipid And Lipoprotein Levels In Rats With Alcohol Induced Liver Injury
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Glycine Modulates Lipid And Lipoprotein Levels In Rats With Alcohol Induced Liver Injury

机译：甘氨酸调节酒精性肝损伤大鼠的脂质和脂蛋白水平

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Glycine is known to have a protective role against alcohol induced liver damage. The aim of our study was to evaluate the effect of glycine on liver and brain lipoproteins in alcohol fed rats. The average total body-weight gain was significantly lower in alcohol-treated rats, but improved on supplementation with glycine. Administering ethanol (7.9 g kg-1 body weight) every day to Wistar rats for 60 days significantly elevated the levels of liver and brain total cholesterol and triglycerides. Serum cholesterol, LDL and VLDL levels were also elevated on administering alcohol, whereas the levels of serum HDL was found to be decreased as compared with the control rats. Simultaneous glycine supplementation (0.6 g kg-1 body weight) during the last 30 days of the experiment to rats administered alcohol, reduced the levels of tissue and serum cholesterol, triglycerides and lipoproteins significantly as compared with the unsupplemented alcohol treated rats. Microscopic examination of alcohol treated rat liver showed inflammatory cell infiltrates and fatty changes, which were reversed on treatment with glycine. Similarly, alcohol treated rat brain demonstrated edema, which was markedly reduced on treatment with glycine. Introduction Most risk factors involved in the causation of liver diseases are directly or indirectly due to the disturbances in lipid and lipoprotein metabolism (1). Ethanol is a powerful inducer of hyperlipidemia both in animals and humans (2). An increase in circulating triglycerides can be produced in fasting individuals after ingestion of ethanol for several hours (3) as well as during administration of alcohol containing diets for several days (4). The accumulation of fat in the liver acts as a stimulus for the secretion of lipoproteins into the blood stream and development of hyperlipidemia (5).Glycine is a dietary non-essential aminoacid that can be readily synthesized from common metabolic intermediates in all organisms. Glycine has multiple roles in many reactions such as gluconeogenesis, purine, haem and chlorophyll synthesis and bile acid conjugation (6). Glycine lowers the rate of gastric emptying of ethanol resulting in the suppression of its absorption from the gastrointestinal tract (7). In an in vivo study of ethanol induced liver injury using the Tsukamoto-French model with a design where alcohol and glycine were given together, glycine lowered ethanol concentration in the stomach and minimized liver damage (8). Glycine derivatives are also known to decrease considerably the activation of lipid peroxidation in stress, reduce the duration of the alarm stage of stress-reaction and limit stress damage to the heart (9). Glycine is said to activate chloride channels in kupffer cells, which hyperpolarizes the cell membrane and blunts intracellular Ca 2+ concentration. Similar to its action in the neurons, glycine also decreases the levels of superoxide ions from neutrophils via glycine gated chloride channels (10). Glycine prevents hepatic cancer and certain melanomas in vivo by inhibiting angiogenesis and endothelial cell proliferation (11). In addition, glycine given orally to schizophrenic patients to facilitate glutamatergic transmission at the level of N-methyl-D-aspartate receptor complex, improved their muscle stiffness and extra pyramidal symptoms (12,13).On the basis of the ever-increasing list of the advantageous role of glycine, we planned the present study. Our aim was to elucidate the lipotropic property of glycine in a rat model with ethanol induced liver injury. Materials and methods Male albino rats weighing 150 to 170 g were procured from the Department of Experimental Medicine, Rajah Muthiah Medical College and Hospital, Annamalai University and were maintained in polypropylene cages in a controlled environment (22-24°C) under 12 h light and dark cycle. Standard pellet diet (Hindustan Lever Ltd., Mumbai, India) and water were provided adlibitum. The animals were cared for as per the principl
机译：已知甘氨酸对酒精引起的肝损伤具有保护作用。我们研究的目的是评估甘氨酸对酒精喂养大鼠肝和脑脂蛋白的影响。酒精治疗的大鼠的平均总体重增加明显较低，但补充甘氨酸后可改善。每天向Wistar大鼠施用乙醇（7.9 g kg-1体重）60天，可显着提高肝脏和大脑总胆固醇和甘油三酸酯的水平。服用酒精后，血清胆固醇，LDL和VLDL水平也升高，而与对照大鼠相比，血清HDL水平降低。与未补充酒精的大鼠相比，在实验的最后30天期间，向服用酒精的大鼠同时补充甘氨酸（0.6 g kg-1体重），显着降低了组织和血清胆固醇，甘油三酸酯和脂蛋白的水平。酒精处理的大鼠肝脏的显微镜检查显示炎性细胞浸润和脂肪变化，甘氨酸处理可逆转。同样，酒精治疗的大鼠大脑显示出水肿，用甘氨酸治疗后水肿明显减轻。引言引起肝脏疾病的大多数危险因素是由于脂质和脂蛋白代谢紊乱直接或间接引起的（1）。乙醇是动物和人类高脂血症的有力诱因（2）。禁食的个体在摄入乙醇数小时后（3）以及服用含酒精饮食几天（4）时，空腹个体中循环甘油三酸酯的增加。肝脏中脂肪的积累可刺激脂蛋白分泌到血流中，并发展为高脂血症（5）。甘氨酸是一种饮食中必需的氨基酸，可以很容易地从所有生物的常见代谢中间体中合成。甘氨酸在许多反应中具有多种作用，例如糖异生，嘌呤，血红素和叶绿素的合成以及胆汁酸的结合（6）。甘氨酸降低了胃中乙醇的排空速度，从而抑制了乙醇从胃肠道的吸收（7）。在使用Tsukamoto-French模型的乙醇诱导的肝损伤的体内研究中，设计了酒精和甘氨酸一起使用的设计，甘氨酸降低了胃中乙醇的浓度，并最大程度地降低了肝损害（8）。还已知甘氨酸衍生物可显着降低应激中脂质过氧化的激活，减少应激反应预警阶段的持续时间，并限制应激对心脏的损害（9）。甘氨酸据说可以激活枯否细胞中的氯离子通道，从而使细胞膜超极化并钝化细胞内Ca 2+的浓度。类似于其在神经元中的作用，甘氨酸还通过甘氨酸门控氯离子通道降低了来自中性粒细胞的超氧离子水平（10）。甘氨酸通过抑制血管生成和内皮细胞增殖而在体内预防肝癌和某些黑色素瘤（11）。此外，向精神分裂症患者口服甘氨酸以促进N-甲基-D-天冬氨酸受体复合物水平的谷氨酸能传递，改善了其肌肉僵硬和额外的锥体束症状（12,13）。关于甘氨酸的有利作用，我们计划了本研究。我们的目的是阐明在乙醇诱导的肝损伤大鼠模型中甘氨酸的亲脂性。材料与方法从安纳马拉大学拉贾穆迪亚医学院和医院实验医学系购得重150至170克的雄性白化病大鼠，并在可控环境（22-24°C）下于12 h光照下饲养在聚丙烯笼中和黑暗的周期。随意提供标准的颗粒饲料（印度孟买的Hindustan Lever Ltd.）和水。按照原则照顾动物

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