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Oral gallic acid improve liver steatosis and metabolism modulating hepatic lipogenic markers in obese mice.
Experimental Gerontology ( IF 3.3 ) Pub Date : 2020-02-18 , DOI: 10.1016/j.exger.2020.110881
Jaciara Neves Sousa 1 , Alanna Fernandes Paraíso 2 , João Marcus Oliveira Andrade 3 , Deborah Farias Lelis 1 , Eloá Mangabeira Santos 3 , Juliana Pinto Lima 4 , Renato Sobral Monteiro-Junior 1 , Marcos Flávio Silveira Vasconcelos D'Angelo 1 , Alfredo Mauricio Batista de Paula 1 , André Luiz Sena Guimarães 1 , Sérgio Henrique Sousa Santos 5
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INTRODUCTION Gallic acid (GA) is a natural endogenous polyphenol found in a variety of fruits, vegetables and wines, with beneficial effects on the energetic homeostasis. AIM The present study aimed to investigate oral gallic acid effects on liver steatosis and hepatic lipogenesis markers in obese mice evaluating new possible molecular related mechanisms. METHODS Twenty-four Swiss male mice were divided into four groups and fed for 60 days with standard diet (ST), standard diet plus gallic acid (ST + GA), high-fat diet (HFD), and high-fat diet plus gallic acid (HFD + GA). We evaluated the relationship between body weight, food intake and serum levels of total cholesterol, triglycerides, insulin, aspartate and alanine transaminases. Liver histology was analyzed by hematoxylin and eosin staining. These results were accompanied by bioinformatics analyses. The acetyl-CoA carboxylase (ACC), sterol regulatory element binding protein-1 (SREBP-1) and fatty acid synthase (FAS) expression was assessed by quantitative real-time reverse transcriptase PCR (qRT-PCR). RESULTS The main findings of the present study showed that GA reduced liver steatosis, body weight and plasma insulin levels. Analyzes of hepatic steatosis related genes expression showed that ACC and FAS mRNA were significantly suppressed in liver of HFD + GA mice. These data was corroborated by bioinformatics analysis. CONCLUSION These data suggest an important clinical application of GA in the prevention of liver diseases.

中文翻译:


口服没食子酸可改善肥胖小鼠的肝脏脂肪变性和代谢调节肝脏脂肪生成标志物。



简介没食子酸 (GA) 是一种天然内源性多酚,存在于多种水果、蔬菜和葡萄酒中,对能量稳态具有有益作用。目的本研究旨在研究口服没食子酸对肥胖小鼠肝脏脂肪变性和肝脏脂肪生成标志物的影响,评估新的可能的分子相关机制。方法瑞士雄性小鼠24只,分为4组,分别采用标准饮食(ST)、标准饮食加没食子酸(ST+GA)、高脂饮食(HFD)、高脂饮食加没食子酸喂养60 d。酸(HFD + GA)。我们评估了体重、食物摄入量和血清总胆固醇、甘油三酯、胰岛素、天冬氨酸和丙氨酸转氨酶水平之间的关系。通过苏木精和伊红染色分析肝脏组织学。这些结果伴随着生物信息学分析。通过定量实时逆转录酶 PCR (qRT-PCR) 评估乙酰辅酶 A 羧化酶 (ACC)、甾醇调节元件结合蛋白-1 (SREBP-1) 和脂肪酸合酶 (FAS) 的表达。结果 本研究的主要结果表明,GA 降低了肝脏脂肪变性、体重和血浆胰岛素水平。肝脂肪变性相关基因表达分析显示,HFD+GA小鼠肝脏中ACC和FAS mRNA显着抑制。这些数据通过生物信息学分析得到证实。结论 这些数据表明 GA 在预防肝病方面具有重要的临床应用。
更新日期:2020-02-20
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