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

DelCurto, Hannah; Wu, Guoyao; Satterfield, Michael C.

Current Opinion in Clinical Nutrition & Metabolic Care: July 2013 - Volume 16 - Issue 4 - p 385–391
doi: 10.1097/MCO.0b013e328361f96d
GENES AND CELL METABOLISM: Edited by Lynette R. Ferguson and Philip Newsholme

Purpose of review Inappropriate 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 findings Maternal 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.

Summary Select 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.

Department of Animal Science, Texas A&M University, College Station, Texas, USA

Correspondence to Michael C. Satterfield, Kleberg Center, 2471 TAMU, Texas A&M University, College Station, TX 77843–2471, USA. Tel: +1 979 845 6448; fax: +1 979 862 2662; e-mail:

© 2013 Wolters Kluwer Health | Lippincott Williams & Wilkins