INVESTIGATING MITOCHONDRIAL METABOLISM IN HIGH-FAT DIET INDUCED FATTY LIVER DISEASE USING WESTERN BLOT ANALYSIS

Abstract

Fatty liver disease (FLD) is the most prevalent liver disorder in industrialized nations. Although FLD is becoming more common as time goes on, there are no approved pharmaceutical treatments currently for the disease. The lack of approved pharmaceutical treatments makes it critical to understand the underlying metabolic defects contributing to disease progression. This study looks at how the disruption of mitochondrial fatty acid transport, through liver-specific knockouts of carnitine acylcarnitine translocase (CACT) impairs mitochondrial and peroxisomal metabolism, leading to liver toxicity. Mice were fed a high-fat, choline-deficient diet (CDAHFD) to induce fatty liver disease, and were treated with fenofibrate, which is a PPAR-α agonist that is known to enhance fatty acid oxidation. Western blot analysis was used to quantify the expression of proteins involved in mitochondrial function, fatty acid transport, and lipid storage. The western blot results are critical because they show how the CACT deficiency impairs mitochondrial fatty acid transport, leading to mitochondrial dysfunction, lipid accumulation, and energy stress. After analysis of the western blots, results do not provide insight indicating that CACT knockout mice show decreased mitochondrial function, leading to the progression of fatty liver disease.