Endocrine Disruptors and Obesity

Curr Obes Rep. 2017 Mar;6(1):18-27. doi: 10.1007/s13679-017-0240-4.

Abstract

Purpose of review: The purpose of this review was to summarise current evidence that some environmental chemicals may be able to interfere in the endocrine regulation of energy metabolism and adipose tissue structure.

Recent findings: Recent findings demonstrate that such endocrine-disrupting chemicals, termed "obesogens", can promote adipogenesis and cause weight gain. This includes compounds to which the human population is exposed in daily life through their use in pesticides/herbicides, industrial and household products, plastics, detergents, flame retardants and as ingredients in personal care products. Animal models and epidemiological studies have shown that an especially sensitive time for exposure is in utero or the neonatal period. In summarising the actions of obesogens, it is noteworthy that as their structures are mainly lipophilic, their ability to increase fat deposition has the added consequence of increasing the capacity for their own retention. This has the potential for a vicious spiral not only of increasing obesity but also increasing the retention of other lipophilic pollutant chemicals with an even broader range of adverse actions. This might offer an explanation as to why obesity is an underlying risk factor for so many diseases including cancer.

Keywords: Adipogenesis; Bisphenol A; Diethylstilbestrol; Endocrine disruptor; Endocrine-disrupting chemicals; Obesity; Obesogen; Paraben; Peroxisome proliferator-activated receptor; Persistent organic pollutants; Tributyltin.

Publication types

  • Review

MeSH terms

  • Adipocytes / drug effects
  • Adipogenesis / drug effects
  • Animals
  • Appetite / drug effects
  • Endocrine Disruptors / pharmacology
  • Endocrine Disruptors / toxicity*
  • Endocrine System Diseases / complications*
  • Female
  • Food Preferences
  • Health Status
  • Humans
  • Mice, Obese
  • Obesity / chemically induced*
  • Organic Chemicals / pharmacology
  • Organic Chemicals / toxicity
  • PPAR gamma / drug effects
  • Pregnancy
  • Prenatal Exposure Delayed Effects
  • Receptors, Aryl Hydrocarbon / drug effects
  • Receptors, Steroid / drug effects
  • Risk Assessment
  • Satiation / physiology

Substances

  • Endocrine Disruptors
  • Organic Chemicals
  • PPAR gamma
  • Receptors, Aryl Hydrocarbon
  • Receptors, Steroid