Environment, Endocrine Disruptors, and Fatty Liver Disease Associated with Metabolic Dysfunction (MASLD)

Abstract

Ecological theories suggest that environmental factors significantly influence obesity risk and related syndemic morbidities, including metabolically abnormal obesity associated with nonalcoholic fatty liver disease (MASLD). These factors encompass anthropogenic influences and endocrine-disrupting chemicals (EDCs), synergistically interacting to induce metabolic discrepancies, notably in early life, and disrupt metabolic processes in adulthood. This review focuses on endocrine disruptors affecting a child's MASLD risk, independent of their role as obesogens and thus regardless of their impact on adipogenesis. The liver plays a pivotal role in metabolic and detoxification processes, where various lipophilic endocrine-disrupting molecules accumulate in fatty liver parenchyma, exacerbating inflammation and functioning as new anthropogenics that perpetuate chronic low-grade inflammation, especially insulin resistance, crucial in the pathogenesis of MASLD.

Keywords: EDCs; MASLD; children; insulin-resistance.

Figure 1

Worldwide distribution of natural and synthetic estrogens in surface waters and rivers [16].

Figure 2

Effects of EDCs during development of MASLD in children. Diagram of how EDCs can affect the fetus, which can be born SGA or IUGR and is exposed to a series of epigenetic, genetic and environmental factors that can cause thyroid disease, obesity, metabolic disorders and NASH to develop in all stages of life.