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Maternal-infant nutrition and development programming of offspring appetite and obesity

Journal

NUTRITION REVIEWS
Volume 78, Issue -, Pages 25-31

Publisher

OXFORD UNIV PRESS INC
DOI: 10.1093/nutrit/nuaa121

Keywords

arcuate nucleus remodeling; hypothalamic arcuate nucleus; maternal obesity; neurogenesis; neuropeptides

Funding

  1. National Institutes of Health [R01DK081756, R01HD054751]
  2. Lundquist Institute Research Committee Bridge and Institutional Use Grant Program [30970-01]

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In the United States and Mexico, the obesity epidemic represents a significant public health problem. Although obesity is often attributed to a Western-style, high-fat diet and decreased activity, there is now compelling evidence that this, in part, occurs because of the developmental programming effects resulting from exposure to maternal overnutrition. Human and animal studies demonstrate that maternal obesity and high-fat diet result in an increased risk for childhood and adult obesity. The potential programming effects of obesity have been partly attributed to hyperphagia, which occurs as a result of increased appetite with reduced satiety neuropeptides or neurons. However, depending on maternal nutritional status during the nursing period, the programmed hyperphagia and obesity can be exacerbated or prevented in offspring born to obese mothers. The underlying mechanism of this phenomenon likely involves the plasticity of the appetite regulatory center and thus presents an opportunity to modulate feeding and satiety regulation and break the obesity cycle.

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