Epigenetic regulation of POMC; implications for nutritional programming, obesity and metabolic disease

Front Neuroendocrinol. 2019 Jul:54:100773. doi: 10.1016/j.yfrne.2019.100773. Epub 2019 Jul 22.

Abstract

Proopiomelanocortin (POMC) is a key mediator of satiety. Epigenetic marks such as DNA methylation may modulate POMC expression and provide a biological link between early life exposures and later phenotype. Animal studies suggest epigenetic marks at POMC are influenced by maternal energy excess and restriction, prenatal stress and Triclosan exposure. Postnatal factors including energy excess, folate, vitamin A, conjugated linoleic acid and leptin may also affect POMC methylation. Recent human studies suggest POMC DNA methylation is influenced by maternal nutrition in early pregnancy and associated with childhood and adult obesity. Studies in children propose a link between POMC DNA methylation and elevated lipids and insulin, independent of body habitus. This review brings together evidence from animal and human studies and suggests that POMC is sensitive to nutritional programming and is associated with a wide range of weight-related and metabolic outcomes.

Keywords: DNA methylation; DOHaD; Epigenetics; Glucose; Insulin; Lipids; Nutrition; Obesity; POMC; Transgenerational.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • DNA Methylation*
  • Epigenesis, Genetic*
  • Female
  • Glucose Metabolism Disorders / etiology
  • Glucose Metabolism Disorders / genetics
  • Glucose Metabolism Disorders / metabolism*
  • Humans
  • Nutritional Physiological Phenomena*
  • Obesity / etiology
  • Obesity / genetics
  • Obesity / metabolism*
  • Pregnancy
  • Prenatal Exposure Delayed Effects / genetics
  • Prenatal Exposure Delayed Effects / metabolism*
  • Pro-Opiomelanocortin / genetics
  • Pro-Opiomelanocortin / metabolism*

Substances

  • Pro-Opiomelanocortin