The Interplay between Endocrine-Disrupting Chemicals and the Epigenome towards Metabolic Dysfunction-Associated Steatotic Liver Disease: A Comprehensive Review

Nutrients. 2024 Apr 11;16(8):1124. doi: 10.3390/nu16081124.

Abstract

Metabolic dysfunction-associated steatotic liver disease (MASLD), described as the most prominent cause of chronic liver disease worldwide, has emerged as a significant public health issue, posing a considerable challenge for most countries. Endocrine-disrupting chemicals (EDCs), commonly found in daily use items and foods, are able to interfere with nuclear receptors (NRs) and disturb hormonal signaling and mitochondrial function, leading, among other metabolic disorders, to MASLD. EDCs have also been proposed to cause transgenerationally inherited alterations leading to increased disease susceptibility. In this review, we are focusing on the most prominent linking pathways between EDCs and MASLD, their role in the induction of epigenetic transgenerational inheritance of the disease as well as up-to-date practices aimed at reducing their impact.

Keywords: DNA methylation; diet; endocrine-disrupting chemicals (EDCs); epigenetic changes; gene–environment interactions; histone alterations; metabolic dysfunction-associated steatotic liver disease (MASLD); microRNAs; transgenerational inheritance.

Publication types

  • Review

MeSH terms

  • Animals
  • Endocrine Disruptors* / adverse effects
  • Epigenesis, Genetic
  • Epigenome
  • Fatty Liver / chemically induced
  • Fatty Liver / genetics
  • Humans
  • Metabolic Diseases / chemically induced
  • Metabolic Diseases / genetics
  • Non-alcoholic Fatty Liver Disease / genetics
  • Receptors, Cytoplasmic and Nuclear / genetics
  • Receptors, Cytoplasmic and Nuclear / metabolism

Substances

  • Endocrine Disruptors
  • Receptors, Cytoplasmic and Nuclear

Grants and funding

This research received no external funding.