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Fetal Metabolic Programming

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Metabolic Syndrome
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Abstract

The global increase in the burden of metabolic-related disease, particularly obesity and type 2 diabetes, means that insights into factors contributing to such conditions are of increasing importance. Evidence from both human studies and animal models suggests that suboptimal conditions in early life may play a role in determining the risk of later metabolic dysfunction. Understanding how later metabolic dysfunction arises at least in part from the early-life environment could lead to exciting new routes to tackle adverse later-life outcomes, either in the index pregnancy via maternal intervention or early in the life of the offspring. Currently, our understanding of the mechanisms of developmental programming of metabolic dysfunction arises primarily from work in animal models, and much remains to be recapitulated and validated in human populations. An ability to tackle metabolic dysfunction early in life and to offset adverse programming of metabolism could prove protective to some degree against many later-life metabolic diseases. Of particular importance is the idea that adverse metabolic phenotypes may not only be seen in the offspring directly exposed to adverse conditions in utero but may also be transmitted or re-propagated across generations. This allows developmental programming of metabolic phenotypes to be viewed on a longer-term basis than a single generation and underscores the idea that early interventions to improve the intrauterine and early postnatal environment could have significant metabolic health benefits to both the children of affected individuals and to future generations.

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Aiken, C.E. (2015). Fetal Metabolic Programming. In: Ahima, R. (eds) Metabolic Syndrome. Springer, Cham. https://doi.org/10.1007/978-3-319-12125-3_14-1

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