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.
Epigenetic regulation of POMC; implications for nutritional programming, obesity and metabolic disease.
T. Candler,Peter Kühnen,Andrew M. Prentice,Matt J Silver
Published 2019 in Frontiers in neuroendocrinology (Print)
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- Publication year
2019
- Venue
Frontiers in neuroendocrinology (Print)
- Publication date
2019-07-01
- Fields of study
Biology, Medicine, Environmental Science
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- Source metadata
Semantic Scholar, PubMed
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