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Effect of gallic acid on high fat diet-induced dyslipidaemia, hepatosteatosis and oxidative stress in rats

机译：Effect of gallic acid on high fat diet-induced dyslipidaemia, hepatosteatosis and oxidative stress in rats

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Gallic acid (GA) is a naturally abundant plant phenolic compound in the human diet and is known to reduce the risk of disease. In this study, the anti-obesity effect of GA in an animal model of diet-induced obesity was investigated. Obesity was induced in male Wistar rats by feeding them a high-fat diet (HFD). GA was given as a supplement at the levels of 50 and 100 mg/kg rat for a period of 10 weeks. The results showed that the body weight, organ weight of the liver and adipose tissue weights of peritoneal and epididymal tissues in the HFD + GA groups were significantly decreased as compared with the HFD group. Serum TAG, phospholipid, total cholesterol, LDL-cholesterol, insulin and leptin levels in the HFD + GA groups were significantly decreased as compared with the HFD group. Histological study showed that the lipid droplets of rats with HFD + GA diets were significantly smaller than those with HFD diets. Hepatic TAG and cholesterol levels in HFD + GA groups were significantly decreased as compared with the HFD group. Moreover, the consumption of GA reduced oxidative stress and GSSG content and enhanced the levels of glutathione, GSH peroxidase, GSH reductase and GSH S-transferase in the hepatic tissue of rats with HFD-induced obesity. These results demonstrate that intake of GA can be beneficial for the suppression of HFD-induced dyslipidaemia, hepatosteatosis and oxidative stress in rats.
机译：没食子酸（GA）是人类饮食中天然富含的植物酚类化合物，已知可以降低疾病风险。在这项研究中，研究了GA在饮食诱发的肥胖动物模型中的抗肥胖作用。通过给雄性Wistar大鼠喂高脂饮食（HFD），可以诱发肥胖。在10周内，以50和100 mg / kg大鼠的水平给予GA作为补充。结果表明，与HFD组相比，HFD + GA组的体重，肝脏器官重量以及腹膜和附睾组织的脂肪含量显着降低。与HFD组相比，HFD + GA组的血清TAG，磷脂，总胆固醇，LDL-胆固醇，胰岛素和瘦素水平显着降低。组织学研究表明，HFD + GA饮食的大鼠的脂滴明显少于HFD饮食的大鼠。与HFD组相比，HFD + GA组的肝TAG和胆固醇水平显着降低。此外，GA的消耗降低了HFD诱发的肥胖大鼠肝组织中的氧化应激和GSSG含量，并增加了谷胱甘肽，GSH过氧化物酶，GSH还原酶和GSH S-转移酶的水平。这些结果表明，摄入GA可以有益于抑制HFD诱导的大鼠血脂异常，肝脂肪变性和氧化应激。

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