Xenobiotic-Induced Aggravation of Metabolic-Associated Fatty Liver Disease.
Julie MassartKarima BegricheAnne CorluBernard FromentyPublished in: International journal of molecular sciences (2022)
Metabolic-associated fatty liver disease (MAFLD), which is often linked to obesity, encompasses a large spectrum of hepatic lesions, including simple fatty liver, steatohepatitis, cirrhosis and hepatocellular carcinoma. Besides nutritional and genetic factors, different xenobiotics such as pharmaceuticals and environmental toxicants are suspected to aggravate MAFLD in obese individuals. More specifically, pre-existing fatty liver or steatohepatitis may worsen, or fatty liver may progress faster to steatohepatitis in treated patients, or exposed individuals. The mechanisms whereby xenobiotics can aggravate MAFLD are still poorly understood and are currently under deep investigations. Nevertheless, previous studies pointed to the role of different metabolic pathways and cellular events such as activation of de novo lipogenesis and mitochondrial dysfunction, mostly associated with reactive oxygen species overproduction. This review presents the available data gathered with some prototypic compounds with a focus on corticosteroids and rosiglitazone for pharmaceuticals as well as bisphenol A and perfluorooctanoic acid for endocrine disruptors. Although not typically considered as a xenobiotic, ethanol is also discussed because its abuse has dire consequences on obese liver.
Keyphrases
- weight loss
- metabolic syndrome
- reactive oxygen species
- type diabetes
- fatty acid
- adipose tissue
- newly diagnosed
- insulin resistance
- genome wide
- obese patients
- risk assessment
- machine learning
- dna methylation
- patient reported outcomes
- bariatric surgery
- gene expression
- weight gain
- big data
- physical activity
- liver fibrosis
- copy number
- patient reported
- intimate partner violence