环境因素导致脂肪肝的发病机制。
Mechanisms of Environmental Contributions to Fatty Liver Disease.
机构信息
Department of Medicine, Division of Gastroenterology, Hepatology and Nutrition, University of Louisville School of Medicine, Louisville, KY, 40202, USA.
University of Louisville Superfund Research Center, University of Louisville, Louisville, KY, 40202, USA.
出版信息
Curr Environ Health Rep. 2019 Sep;6(3):80-94. doi: 10.1007/s40572-019-00232-w.
PURPOSE
Fatty liver disease (FLD) affects over 25% of the global population and may lead to liver-related mortality due to cirrhosis and liver cancer. FLD caused by occupational and environmental chemical exposures is termed "toxicant-associated steatohepatitis" (TASH). The current review addresses the scientific progress made in the mechanistic understanding of TASH since its initial description in 2010.
RECENT FINDINGS
Recently discovered modes of actions for volatile organic compounds and persistent organic pollutants include the following: (i) the endocrine-, metabolism-, and signaling-disrupting chemical hypotheses; (ii) chemical-nutrient interactions and the "two-hit" hypothesis. These key hypotheses were then reviewed in the context of the steatosis adverse outcome pathway (AOP) proposed by the US Environmental Protection Agency. The conceptual understanding of the contribution of environmental exposures to FLD has progressed significantly. However, because this is a new research area, more studies including mechanistic human data are required to address current knowledge gaps.
目的
脂肪肝疾病（FLD）影响了全球超过 25%的人口，并可能由于肝硬化和肝癌导致与肝脏相关的死亡率。由职业和环境化学暴露引起的 FLD 被称为“毒物相关脂肪性肝炎”（TASH）。本综述针对自 2010 年首次描述以来，在 TASH 的机制理解方面取得的科学进展进行了探讨。
最近的发现
挥发性有机化合物和持久性有机污染物的新作用模式包括：（i）内分泌、代谢和信号转导干扰假说；（ii）化学-营养相互作用和“双打击”假说。然后，这些关键假说在美国环境保护署提出的脂肪变性不良结局途径（AOP）的背景下进行了综述。人们对环境暴露对 FLD 贡献的概念理解已经取得了重大进展。然而，由于这是一个新的研究领域，需要更多包括机制性人体数据的研究来解决当前的知识空白。
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