期刊文献+

二甲双胍对非酒精性脂肪肝的缓解与AMPK-G0S2信号通路的关系 被引量:4

Improvement of Metformin on NAFLD and its Relationship with AMPK-G0S2 Pathway
下载PDF
导出
摘要 目的:探讨二甲双胍对G0期G1期转换基因2(G0S2)的调控作用在非酒精性脂肪肝(NAFLD)治疗中的作用机制。方法:在动物水平12只雄性ob/ob小鼠随机分为二甲双胍组,对照组。在小鼠药物处理期间测量小鼠体重,实验结束时称量小鼠的进食量,肝脏的重量,检测肝脏组织中脂质含量。实时荧光定量PCR和Western blotting在RNA水平和蛋白水平检测小鼠肝脏组织中AMPK信号通路相关分子以及G0S2的变化。结果:二甲双胍组ob/ob小鼠体重明显低于对照组,且摄食量没有明显差异。二甲双胍组ob/ob小鼠肝脏组织重量以及脂质含量均低于对照组。在分子水平上二甲双胍显著激活ob/ob小鼠肝脏组织中AMPK信号通路且下调G0S2蛋白表达。结论:二甲双胍通过激活AMPK信号通路下调G0S2的表达,促进脂肪分解进而有效的缓解NAFLD。 Objective: To investigate the effect of metformin on the regulation of G0,G1 phase 2(G0S2) in the treatment of nonalcoholic fatty liver disease(NAFLD).Methods: 12 male ob/ob mice were randomly divided into two groups,the metformin group and the control group.Mice were measured at the time of drug treatment,and the amount of food and liver weight were measured at the end of the experiment,and the lipid content in liver tissue was detected.Real time fluorescent quantitative PCR and blotting Western were used to detect the changes of AMPK signaling pathway related molecules and G0S2 in the liver tissues of mice in the RNA level and protein level.Results: The weight of ob/ob mice in the metformin group was significantly lower than that in the control group,and there was no significant difference between the two groups.The weight and lipid content of liver tissue in ob/ob mice were lower than those in control group.At the molecular level,metformin significantly activated the AMPK signaling pathway in liver tissue of ob/ob mice and down regulated the expression of G0S2 protein.Conclusion: The effect of metformin on the expression of G0S2 by activating the AMPK signaling pathway promotes the effective remission of NAFLD.
出处 《中国医药导刊》 2016年第4期401-402,共2页 Chinese Journal of Medicinal Guide
关键词 二甲双胍 非酒精性脂肪肝 AMPK G0S2 Metformin Non-alcoholic fatty liver AMPK G0S2
  • 相关文献

参考文献13

  • 1Byrne CD,Targher G. NAFLD: a multisystem disease[J]. J Hepatol, 2015, 62 (1Suppl): S47-64. 被引量:1
  • 2Boussageon R,Gueyffier F,Cornu C. Metformin as firstline treatment for type 2diabetes: are we sure?[J]. BMJ, 2016, 352:6748. 被引量:1
  • 3Klein JD,Wang Y,Blount, MA, et al. Metformin, an AMPK activator, stimulatesthe phosphorylation of Aquaporin 2 and Urea Transporter A1 in Inner MedullaryCollecting Ducts[J]. Am J Physiol Renal Physiol, 2016, ajprenal 00102 2016. 被引量:1
  • 4Trappoliere M,Tuccillo C,Federico A, et al. The treatment of NAFLD[J]. Eur RevMed Pharmacol Sci, 2005, 9(5):299-304. 被引量:1
  • 5Hardie DG. Sensing of energy and nutrients by AMP-activated protein kinase[J].Am J Clin Nutr, 2011, 93(4): 891S-6. 被引量:1
  • 6Yang XY,Lu X,Lombes M, et al. The G(0)/G(1) Switch Gene 2 RegulatesAdipose Lipolysis through Association with Adipose Triglyceride Lipase[J]. Cellmetabolism, 2010, 11(3):194-205. 被引量:1
  • 7Choudhury J,Sanyal AJ. Insulin resistance and the pathogenesis of nonalcoholicfatty liver disease[J]. Clin Liver Dis,2004, 8(3):575-594. 被引量:1
  • 8Mazza A,Fruci B,Garinis GA, et al. The role of metformin in the management ofNAFLD[J]. Exp Diabetes Res, 2012, 2012:716404. 被引量:1
  • 9Heckmann BL,Zhang X,Xie X, et al. Defective adipose lipolysis and altered globalenergy metabolism in mice with adipose overexpression of the lipolytic inhibitor G0/G1switch gene 2 (G0S2)[J]. The Journal of biological chemistry, 2014,289(4):1905-1916. 被引量:1
  • 10Ma T,Lopez-Aguiar AG,Li A, et al. Mice lacking G0S2 are lean and coldtolerant[J]. Cancer biology & therapy, 2014,15(5):643-50. 被引量:1

同被引文献47

引证文献4

二级引证文献22

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部