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Nat Rev Endocrinol. 2017 Aug;13(8):445-457. doi: 10.1038/nrendo.2017.42. Epub 2017 May 19.

Endocrine-disrupting chemicals and fatty liver disease.

Author information

1
Department of Molecular and Cellular Biology, Baylor College of Medicine.
2
Center for Precision Environmental Health, Baylor College of Medicine.
3
Dan L. Duncan Cancer Center, Baylor College of Medicine.
4
Department of Medicine, Baylor College of Medicine, 1 Baylor Plaza, Houston, Texas 77030, USA.

Abstract

A growing epidemic of nonalcoholic fatty liver disease (NAFLD) is paralleling the increase in the incidence of obesity and diabetes mellitus in countries that consume a Western diet. As NAFLD can lead to life-threatening conditions such as cirrhosis and hepatocellular carcinoma, an understanding of the factors that trigger its development and pathological progression is needed. Although by definition this disease is not associated with alcohol consumption, exposure to environmental agents that have been linked to other diseases might have a role in the development of NAFLD. Here, we focus on one class of these agents, endocrine-disrupting chemicals (EDCs), and their potential to influence the initiation and progression of a cascade of pathological conditions associated with hepatic steatosis (fatty liver). Experimental studies have revealed several potential mechanisms by which EDC exposure might contribute to disease pathogenesis, including the modulation of nuclear hormone receptor function and the alteration of the epigenome. However, many questions remain to be addressed about the causal link between acute and chronic EDC exposure and the development of NAFLD in humans. Future studies that address these questions hold promise not only for understanding the linkage between EDC exposure and liver disease but also for elucidating the molecular mechanisms that underpin NAFLD, which in turn could facilitate the development of new prevention and treatment opportunities.

PMID:
28524171
DOI:
10.1038/nrendo.2017.42
[Indexed for MEDLINE]
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