Early origins of obesity and developmental regulation of adiposity

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Abstract

Whilst overweight and obesity result in significant health problems in childhood and adulthood, their origins may lie in earlier life experiences from the nutritional environment of the periconceptional, in utero and postnatal periods. Epidemiological data from human populations show that changes in maternal nutrition during different phases of pregnancy affects the long term health of offspring. Importantly in the context of contemporary populations, maternal overnutrition and obesity also influence offspring health and may induce long term changes which predispose offspring to insulin resistance, obesity and metabolic syndrome in later life. Although changes in maternal nutrition can alter fetal adiposity without overall changes in birthweight, obese mothers are more likely to have large for gestational age babies and these offspring are more prone to becoming overweight and obese in later life. In addition to the effects of the maternal nutritional environment, accelerated growth in the early postnatal period, particularly when proceeded by fetal growth restriction, can be detrimental to long term health and increase the risks of obesity and Type 2 diabetes, consequences similar to those following rapid and early increases in body mass index in childhood. Key pathways of fetal programming include those mediated through glucocorticoids, with their vital role in developmental regulation of adipose tissue, appetite regulation and energy homeostasis regulated by the hypothalamus, and the neurohormones insulin and leptin influencing the actions of neuropeptides in the hypothalamic nuclei. A better understanding of these processes may provide opportunities for the prevention of obesity and improved public health.

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Ojha, S., & Budge, H. (2017). Early origins of obesity and developmental regulation of adiposity. In Adipose Tissue Biology: Second Edition (pp. 427–456). Springer International Publishing. https://doi.org/10.1007/978-3-319-52031-5_12

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