Early origins of obesity and developmental regulation of adiposity

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, such as from the Dutch “Hunger Winter” studies, show that maternal undernutrition 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 foetal adiposity without overall changes in birthweight, obese mothers are more likely to have large gestational age babies, and these offspring are more likely to become 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 preceded by foetal 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 BMI in childhood. Key pathways of foetal 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.