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Abstract Details
Role of Endocrine-Disrupting Chemicals in the Pathogenesis of Non-Alcoholic Fatty Liver Disease: A Comprehensive Review
Int J Mol Sci. 2021 May 1;22(9):4807. doi: 10.3390/ijms22094807.
Raquel Cano1, José L Pérez1, Lissé Angarita Dávila2, Ángel Ortega1, Yosselin Gómez1, Nereida Josefina Valero-Cedeño3, Heliana Parra1, Alexander Manzano1, Teresa Isabel Véliz Castro3, María P Díaz Albornoz1, Gabriel Cano4, Joselyn Rojas-Quintero5, Maricarmen Chacín6, Valmore Bermúdez6
Author information
1Endocrine and Metabolic Diseases Research Center, School of Medicine, University of Zulia, Maracaibo 4004, Venezuela.
2Escuela de Nutrición y Dietética, Facultad de Medicina, Universidad Andres Bello, Sede Concepción 4260000, Chile.
3Carrera de Laboratorio Clínico, Facultad de Ciencias de la Salud, Universidad Estatal del Sur de Manabí, Jipijapa E482, Ecuador.
5Division of Pulmonary and Critical Care Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA.
6Facultad de Ciencias de la Salud, Universidad Simón Bolívar, 080002 Barranquilla, Colombia.
Abstract
Non-alcoholic fatty liver disease (NAFLD) is considered the most common liver disorder, affecting around 25% of the population worldwide. It is a complex disease spectrum, closely linked with other conditions such as obesity, insulin resistance, type 2 diabetes mellitus, and metabolic syndrome, which may increase liver-related mortality. In light of this, numerous efforts have been carried out in recent years in order to clarify its pathogenesis and create new prevention strategies. Currently, the essential role of environmental pollutants in NAFLD development is recognized. Particularly, endocrine-disrupting chemicals (EDCs) have a notable influence. EDCs can be classified as natural (phytoestrogens, genistein, and coumestrol) or synthetic, and the latter ones can be further subdivided into industrial (dioxins, polychlorinated biphenyls, and alkylphenols), agricultural (pesticides, insecticides, herbicides, and fungicides), residential (phthalates, polybrominated biphenyls, and bisphenol A), and pharmaceutical (parabens). Several experimental models have proposed a mechanism involving this group of substances with the disruption of hepatic metabolism, which promotes NAFLD. These include an imbalance between lipid influx/efflux in the liver, mitochondrial dysfunction, liver inflammation, and epigenetic reprogramming. It can be concluded that exposure to EDCs might play a crucial role in NAFLD initiation and evolution. However, further investigations supporting these effects in humans are required.