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Nutritional programming of the metabolic syndrome

Nature Reviews Endocrinology volume 5, pages 604–610 (2009)Cite this article

Abstract

The primary markers of the metabolic syndrome are central obesity, insulin resistance and hypertension. In this review, we consider the effect of changes in maternal nutrition during critical windows in fetal development on an individual's subsequent predisposition to the metabolic syndrome. The fetal origins of obesity, cardiovascular disease and insulin resistance have been investigated in a wide range of epidemiological and animal studies; these investigations highlight adaptations made by the nutritionally manipulated fetus that aim to maintain energy homeostasis to ensure survival. One consequence of such developmental plasticity may be a long term re-setting of cellular energy homeostasis, most probably via epigenetic modification of genes involved in a number of key regulatory pathways. For example, reduced maternal–fetal nutrition during early gestation to midgestation affects adipose tissue development and adiposity of the fetus by setting an increased number of adipocyte precursor cells. Importantly, clinically relevant adaptations to nutritional challenges in utero may only manifest as primary components of the metabolic syndrome if followed by a period of accelerated growth early in the postnatal period and/or if offspring become obese.

Key Points

  • Foundations for the metabolic syndrome may be laid down in very early life as a consequence of changes in dietary supply to the rapidly growing conceptus and/or postnatal offspring

  • Critical windows of development, during which the fetus is susceptible to nutritional programming, must be considered in the etiology of the metabolic syndrome

  • A common epigenetic mechanism is fundamental to developmental programming of endocrine balance and cellular energy metabolism; the latter determines the partition of energy between catabolism and energy storage

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Figure 1: The effects on reproductive outcomes of the gross differences in maternal diet between women in developed and developing countries.88,27,29
Figure 2: Critical windows for fetal organogenesis and changes in placental and body weight between conception and early postnatal life, in a range of species.
Figure 3: The contributory role of the maternal–fetal environment in the developmental programming of cellular energy metabolism in favor of lipid storage.

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Acknowledgements

The authors acknowledge the support of the European Union Sixth Framework Program for Research and Technical Development of the European Community—The Early Nutrition Programming Project (FOOD-CT-2005-007,036)—in their research.

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  1. Division of Human Development, Early Life Nutrition Research Unit, Academic Child Health, School of Clinical Sciences, University Hospital, Nottingham, UK

    Michael E. Symonds, Sylvain P. Sebert, Melanie A. Hyatt & Helen Budge

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Symonds, M., Sebert, S., Hyatt, M. et al. Nutritional programming of the metabolic syndrome. Nat Rev Endocrinol 5, 604–610 (2009). https://doi.org/10.1038/nrendo.2009.195

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