4.2 Review

Nutrition and reproduction: links to epigenetics and metabolic syndrome in offspring

Journal

Publisher

LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/MCO.0b013e328361f96d

Keywords

epigenetics; fetal programming; metabolic disease; nutrition; pregnancy

Funding

  1. National Institutes of Health [1R21 HD049449]
  2. National Research Initiative Competitive Grants from the Animal Reproduction Program [2008-35203-19120]
  3. Animal Growth & Nutrient Utilization Program of the USDA National Institute of Food and Agriculture [2008-35206-18764, 2009-35206-05211]
  4. Texas AgriLife Research [H-8200]

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Purpose of reviewInappropriate exposure of gametes and/or products of conception to nutritional imbalance alters critical metabolic set points in the offspring and increases propensity to disease. This review will focus on recent findings highlighting clear links to epigenetic modifications in response to dietary manipulations as well as nutritional strategies with the potential to mitigate the effects of an otherwise poor nutritional environment.Recent findingsMaternal nutritional imbalance, either through global nutritional manipulation or deficiencies in select nutrients, predisposes the offspring to metabolic disease. Disease susceptibility is linked to global and/or specific modifications of the epigenome at key metabolic regulatory genes. Paternal nutritional imbalance also increases the likelihood of metabolic disease in offspring through similar epigenetic mechanisms. Finally, dietary intervention with select nutrients has been shown to ameliorate postnatal disease phenotypes in offspring, although the exact molecular mechanisms have not been elucidated.SummarySelect nutrients, such as amino acids and vitamins, not only serve as building blocks for growth but also mediate a myriad of physiological functions, including providing substrates for DNA synthesis. These nutrients hold great promise as intervention strategies to combat a suboptimal developmental environment.

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