PPARα agonist WY-14,643 induces adipose atrophy and fails to blunt chronic ethanol-induced hepatic fat accumulation in mice lacking adipose FGFR1

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Excessive consumption of alcohol cause alcohol-related liver disease (ALD). Accompanied by the elimination process of alcohol via various metabolic mechanisms, ALD progresses from alcoholic steatosis (fatty liver) to alcoholic steatohepatitis (hepatic inflammation). Chronic hepatic inflammation can eventually lead to fibrosis, cirrhosis, and even hepatocellular cancer. Alcohol toxicity is linked to alcohol metabolism. In general, alcohol metabolism is achieved through oxidative pathways involving alcohol dehydrogenase (ADH), cytochrome P450 (CYP) enzymes mainly CYP2E1, and catalase. The consequences of alcohol metabolism include hypoxia in the liver; the formation of harmful adducts; generation of reactive oxygen species (ROS); impaired metabolic processes promoting the development of fatty liver.


The author manuscript is available from PMC at https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8549793/. The version of record is available from the publisher at https://doi.org/10.1016/j.bcp.2021.114678. Copyright © 2021 Elsevier.