Angrish Michelle M, Kaiser Jonathan Phillip, McQueen Charlene A, Chorley Brian N
*National Health and Environmental Effects Research Laboratory, Office of Research and Development (ORD), United States Environmental Protection Agency (US EPA), Research Triangle Park, North Carolina 27709;
United States Environmental Protection Agency (US EPA), National Center for Environmental Assessment, Office of Research and Development (ORD), Cincinnati, Ohio 45268.
Toxicol Sci. 2016 Apr;150(2):261-8. doi: 10.1093/toxsci/kfw018. Epub 2016 Mar 15.
Hepatic steatosis is a condition were fat accumulates in the liver and it is associated with extra-hepatic diseases related to metabolic syndrome and systemic energy metabolism. If not reversed, steatosis can progress to steatohepatitis and irreversible stages of liver disease including fibrosis, cirrhosis, hepatocellular carcinoma, and death. From a public health standpoint, identifying chemical exposures that may be factors in steatosis etiology are important for preventing hepatotoxicity and liver disease progression. It is therefore important to identify the biological events that are key for steatosis pathology mediated by chemical exposure. In this review, we give a current overview of the complex biological cascades that can disrupt lipid homeostasis in hepatocytes in the context of 4 apical key events central to hepatic lipid retention: hepatic fatty acid (FA) uptake,de novoFA and lipid synthesis, FA oxidation, and lipid efflux. Our goal is to review these key cellular events and visually summarize them using a network for application in pathway-based toxicity testing. This effort provides a foundation to improve next-generation chemical screening efforts that may be used to prevent and ultimately reverse the growing incidence of fatty liver disease in our population.
肝脂肪变性是一种脂肪在肝脏中蓄积的病症,它与代谢综合征和全身能量代谢相关的肝外疾病有关。如果不逆转,脂肪变性可进展为脂肪性肝炎以及肝病的不可逆阶段,包括肝纤维化、肝硬化、肝细胞癌,甚至死亡。从公共卫生的角度来看,识别可能是脂肪变性病因的化学暴露因素对于预防肝毒性和肝病进展至关重要。因此,识别化学暴露介导的脂肪变性病理关键生物学事件很重要。在本综述中,我们概述了当前复杂的生物学级联反应,这些反应在肝脏脂质潴留的4个关键顶端事件(肝脂肪酸(FA)摄取、FA和脂质从头合成、FA氧化以及脂质流出)的背景下可破坏肝细胞中的脂质稳态。我们的目标是回顾这些关键细胞事件,并使用网络直观地总结它们,以便应用于基于通路的毒性测试。这项工作为改进下一代化学筛选工作奠定了基础,这些筛选工作可用于预防并最终扭转我国人群中脂肪肝疾病发病率不断上升的趋势。