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Nutritional programming of hypothalamic development: critical periods and windows of opportunity

International Journal of Obesity Supplements volume 2, pages S19S24 (2012) | Download Citation

This article was published as part of a supplement funded with an unrestricted educational contribution from Desjardins Sécurité Financière.

Abstract

Obesity is increasing at an alarming rate throughout the world, particularly among children. Epidemiological and experimental data have suggested that suboptimal nutrition and growth during prenatal and/or postnatal life can have a significant role in the development of obesity and related diseases. Similarly, exposure to malnutrition during perinatal life can result in lifelong metabolic disorders. Although the precise biological mechanisms governing metabolic programming have not been fully elucidated, there is growing evidence that obesity and other metabolic diseases may result from a change in the underlying developmental program of the hypothalamic pathways that regulate energy balance. The hypothalamus undergoes tremendous growth beginning in the embryonic period and continuing through adolescence, and an alteration in perinatal nutrition can affect various developmental processes, including neurogenesis and axon growth, which can lead to abnormal hypothalamic development. Metabolic hormones, particularly leptin, are capable of transmitting signals to the developing hypothalamus in response to alterations in the nutritional environment and may underlie potential maladaptive responses to early metabolic perturbations. A better understanding of the optimal perinatal hormonal and nutritional environment during hypothalamic development may help ameliorate and reverse the metabolic malprogramming of the fetus and/or neonate.

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Acknowledgements

I thank the members of my laboratory for their active participation in the studies discussed in this review. Research in my laboratory has been funded by grants from the National Institute of Health (Grant DK84142), the ‘Fondation pour la Recherche Médicale’ and Institut Danone, the EU FP7 integrated project (Grant Agreement No. 266408, ‘Full4Health’), and the ‘Agence Nationale de la Recherche’ (Grants ANR-08-JCJC-0055-01 and ANR-11-BSV1-021-02).

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Affiliations

  1. The Saban Research Institute, Neuroscience Program, Children's Hospital Los Angeles, University of Southern California, Los Angeles, CA, USA

    • S G Bouret
  2. Inserm, Jean-Pierre Aubert Research Center, U837, Neurobese Lab, University Lille 2, Lille, France

    • S G Bouret

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The author declares no conflict of interest.

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Correspondence to S G Bouret.

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DOI

https://doi.org/10.1038/ijosup.2012.17