Tian Wei . Liraglutide Improves The Symptoms of Non-alcoholic Fatty Liver Disease by Regulating Fatty Acid β-oxidation[J]. Journal of Kunming Medical University, 2016, 37(02).
Citation: Tian Wei . Liraglutide Improves The Symptoms of Non-alcoholic Fatty Liver Disease by Regulating Fatty Acid β-oxidation[J]. Journal of Kunming Medical University, 2016, 37(02).

Liraglutide Improves The Symptoms of Non-alcoholic Fatty Liver Disease by Regulating Fatty Acid β-oxidation

  • [Abstract]Objective To investigate and analyze the effect of Liraglutide on the expression of fatty acids β-oxidation key enzymes,Acyl Coenzyme A Oxidase1(ACOX1)and Peroxisome Proliferators-Activated Receptor α(PPARα),in high fat food induced Non-alcoholic Fatty Liver Disease( NAFLD)in rats,in order to investigate whether it can treat NAFLD through the above ways.Methods Severty rats were randomly divided into control, model and liraglutide group,after NAFLD model was successfully established,liraglutide treatment group received liraglutide 60 ug/(kg.d)treatment, model group and control group were given saline injections. 4 weeks and 8 weeks later,the rats were sacrificed to detect the correlated indexes.Results Liver pathology showed that cells were smooth and arranged regularly,cell size was uniform,and no fatty infiltration in control group,the presence of significant liver fat deposition in model group,4 weeks after treatment,liver fat deposition significantly reduced, 8 weeks after treatment,liver fat deposition significantly reduced further,but there was still a certain difference compared to the control group. After treatment,liver function and blood lipids were significantly improved;4 weeks after treatment,compared with the model group,in the treatment group liver PPARα and ACOX1 protein and mRNA expression increased, but the difference was not statistically significant, 8 weeks after treatment,both of them were significantly increased(P<0.05). Conclusion Liraglutide can significantly improve the high-fat diet-induced lipid,improve liver function, which may be related with the upregulation of fatty acids β-oxidation key enzymes PPARα and ACOX1, thus contributing to the discharge of the accumulated fatty acid in liver.
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