Investigation of Mitophagy Relation Genes Expression in Mice Fed a High-Fat Diet and Exercised

Abstract

Abstract Adipose tissue plays an essential role as both an energy store and an endocrine organ in metabolism. İncreased adipose tissue leads to a low-grade chronic inflammation that can change systemin inflammation in obesity. İncreased inflammation and hypoxia cause mitochondrial dysfunction and trigged mitochondrial autophagy (mitophagy). Therefore, we investigated the mitophagy-related genes ATG3, MFN1, PINK1, and PARKIN gene expression levels in mice fed a high-fat diet and exercised. The animal model was created as a control, obese, and exercise group. The obese and exercise group received a 60% kcal high-fat diet. The exercise group was exercised starting the 6th week of study until sacrificed. The control group received %10 kcal high-fat diet and all mice remained on the same diet until sacrificed. Expression levels were determined by using a Real-Time PCR system in liver and adipose tissue. ATG3 and PINK1 expressions were significantly increased in the liver and adipose tissues of the exercise group compared to the control and obese groups (p<0.05). MFN1 and PARKIN expressions increased significantly in the liver tissues of the exercise group compared to the control group (p<0.05). PARKIN and MFN1 expressions were significantly decreased in the liver of the obese group compared to the control group (p<0.05). This study is a pioneer in examining the expressions of mitophagy-related genes PINK1, PARKIN, MFN1, and ATG3 and will contribute to the literature in this sense.