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Am. J. Biomed. Sci. 2020,12(4),257-266;doi:10.5099/aj200400257
Received:08 May 2020; | Revised:23 July 2020; | Accepted:12 December 2020

 

Compensative Response Elicited towards Steatosis in High Fat Diet-induced Non-alcoholic Fatty Liver Disease in Rats

 

Magda Abdel Ghany Megahed a,*, Safia Mohamed Hassanb, Mohamed Mohamed Shamsia c, Osama Ghazy badr a , Shimaa A Mahmoud a

a Department of Biochemistry, Medical Research Institute, Alexandria University, Egypt.

b Department of Histochemistry and Cell Biology, Medical Research Institute, Alexandria University,  Egypt.

c Department of Clinical and Experimental Internal Medicine, Medical Research Institute, Alexandria University, Egypt.

*Corresponding Author

Magda Abdel Ghany Megahed

Department of Biochemistry,

Medical Research Institute,

Alexandria University

Egypt

Email: magda.megahad@alexu.edu.eg

Tel.: +20 3 4282331/73

fax: +20 3 4283719

 

Abstract

Non-alcoholic fatty liver disease (NAFLD) is the condition in which hepatic fat accumulation is present after exclusion of all other causes of hepatic steatosis such as liver disease caused by other factors, excessive alcohol consumption, and other conditions that may lead to hepatic steatosis. Structural and functional alterations in mitochondria contribute to the pathogenesis of NAFLD. In this study, we investigated the impact of high fat diet on gene expression of SIRT1 and PGC-1α in experimental non-alcoholic fatty liver disease. The results showed upregulation of both PGC-1α and SIRT1 gene expression in fatty liver group in comparison to control group. This finding is explained as an adaptive response elicited by the hepatocytes against the high fat diet induced-steatosis.

 

Keywords: Fatty liver; mitochondrial biogenesis; reactive oxygen species; steatosis; steatohepatitis; SIRT1; PGC-1α; TNFα

 

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