Fatty liver induction negatively affects mitochondrial respiratory function in female rats

Supervisor Name

Johnny Stiban

Supervisor Email

Jstiban@birzeit.edu

University

Birzeit University

Research field

Medical Sciences

Bio

Professor Faculty Member - Department Of Biology And Biochemistry PhD University of Maryland

Description

Chronic liver diseases (CLDs) represent a large group of diseases that damage livers. Alcoholic liver disease (ALD), non-alcoholic fatty liver disease (NAFLD), chronic viral hepatitis, and other genetic and autoimmune causes are among the underlying etiologies of CLDs. CLDs affected approximately 1.5 billion people in 2017. Obesity and alcohol use have emerged as significant risk factors for liver disease. They are predicted to influence CLD epidemiology in the future and account for an increasing proportion of deaths. Because of the prevalence of CLDs, many studies and research have been conducted at the molecular level to investigate the mechanisms, onset of CLDs, and factors that play a role in increasing or decreasing CLD incidence. NAFLD is one of the diseases that causes fat accumulation and liver cell damage. We plan to study the development of NAFLD in animal models. Studying diseases in animal models constitutes a cornerstone of understanding the causes and mechanisms of multiple human diseases. Many factors contribute to the development of fatty liver in animal models. Here, we propose to use ethionine injection and high-fat diets to cause triacylglycerol (TAG) accumulation and, as a result, NAFLD. After the induction of NAFLD, We will use Blue-native polyacrylamide gel electrophoresis (BN-PAGE) to study the effects of NAFLD on the activities of respiratory complexes in the mitochondria. We propose that the induction of NAFLD will induce molecular changes at the level of mitochondria rendering them unable to properly function.