Institut NUMECAN (Nutrition Metabolisms and Cancer), UMR_A 1341, UMR_S 1241, INSERM, University Rennes, INRAE, F-35000 Rennes, France.
Int J Mol Sci. 2022 Jan 19;23(3):1062. doi: 10.3390/ijms23031062.
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.
代谢相关脂肪性肝病(MAFLD)常与肥胖相关,它包含了广泛的肝脏病变,包括单纯性脂肪肝、脂肪性肝炎、肝硬化和肝细胞癌。除了营养和遗传因素外,不同的外源性物质,如药物和环境毒素,被怀疑会加重肥胖人群的 MAFLD。更具体地说,在治疗患者或暴露个体中,先前存在的脂肪肝或脂肪性肝炎可能会恶化,或者脂肪肝可能会更快地进展为脂肪性肝炎。外源性物质加重 MAFLD 的机制仍知之甚少,目前正在深入研究中。然而,先前的研究指出了不同代谢途径和细胞事件的作用,如从头合成脂肪生成的激活和线粒体功能障碍,这些大多与活性氧过度产生有关。本综述介绍了用一些典型化合物获得的现有数据,重点是药物中的皮质类固醇和罗格列酮以及内分泌干扰物中的双酚 A 和全氟辛酸。尽管乙醇通常不被认为是一种外源性物质,但由于其滥用对肥胖肝脏有严重后果,因此也进行了讨论。