Impact of Metabolic disrupting chemicals on redox homeostasis, energy sensors, receptor modulation, and hormone metabolism: A comparative account in Teleost and mammalian model organisms

Abstract

Endocrine-disrupting chemicals (EDCs) may mimic the endogenous neuroendocrine and endocrine messengers and interfere with developmental, reproductive, immune, metabolic and other physiological functions. Modulation of basal metabolic rate, energy metabolism, food intake and engorgement by endocrine disruptors may lead to loss of metabolic equilibrium. EDC-induced loss of metabolic homeostasis and obesity gave rise to the concept of metabolic-disrupting chemicals (MDC) and environmental obesogens. Elevated oxidative stress, alterations in the circadian clock, and energy-sensing homeostasis are some of the major pathophysiological conditions implicated in promoting metabolic disruption. Reportedly, fish are the most vulnerable candidate due to their direct exposure to metabolic disruptors in aquatic habitats. Though limited, studies conducted using piscine models have helped to identify MDCs in the aquatic environment. Notably, the molecular mechanisms through which MDCs can negatively influence the metabolism of hormones, epigenetic alteration, gut dysbiosis, and changes in endocrine and metabolic receptor expression and functions have recently gained considerable attention. In this review, we provide an update on the impact of MDCs on the initiators, cellular mediators, and hormone receptors related to the maintenance of metabolic homeostasis, with particular emphasis on fish models.

Keywords

• Reactive oxygen species
• SIRT1/AMPK/PGC
• PPAR
• Estrogen receptor
• Hormone metabolism
• Metabolic disruption