Abstract
The global prevalence of obesity has increased markedly over the last two decades with over 50% of all adults in the UK and USA classified as overweight or obese. Furthermore, the prevalence of obesity in children has risen by over 40% in the last 16 years. Obesity results from the interaction of many factors, including genetic, metabolic, behavioral, and environmental influences. However, the rate at which obesity is increasing suggests that environmental and behavioral influences, rather than genetic changes, have fueled the epidemic. In this context, it is of particular relevance that epidemiological and experimental studies have highlighted a relationship between the periconceptual, fetal and early infant phases of life and the subsequent development of adult adiposity. This relationship; the “developmental origins of health and disease” (DOHaD) model, speculates that the fetus adapts to adverse environmental cues in utero with permanent readjustments in homeostatic systems to aid survival. However, these adaptations, known as predictive adaptive responses, may ultimately be disadvantageous in postnatal life and may lead to an increased risk of chronic non-communicable disease in adulthood. This review summarises recent work in animal models and observations in the clinical and epidemiological settings on the in-utero origins of obesity and related metabolic disorders.
Keywords: MAPK pathways, growth hormone, dexamethasone, DOHaD hypotheses, maternal low protein
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