Purpose of review: A growing body of epidemiological and experimental data indicate that nutritional or environmental stressors during early development can induce long-term adaptations that increase risk of obesity, diabetes, cardiovascular disease, and other chronic conditions-a phenomenon termed "developmental programming." A common phenotype in humans and animal models is altered body composition, with reduced muscle and bone mass, and increased fat mass. In this review, we summarize the recent literature linking prenatal factors to future body composition and explore contributing mechanisms.
Recent findings: Many prenatal exposures, including intrauterine growth restriction, extremes of birth weight, maternal obesity, and maternal diabetes, are associated with increased fat mass, reduced muscle mass, and decreased bone density, with effects reported throughout infancy and childhood, and persisting into middle age. Mechanisms and mediators include maternal diet, breastmilk composition, metabolites, appetite regulation, genetic and epigenetic influences, stem cell commitment and function, and mitochondrial metabolism. Differences in body composition are a common phenotype following disruptions to the prenatal environment, and may contribute to developmental programming of obesity and diabetes risk.
Keywords: Adiposity; Bone mass; Developmental programming; Epigenetics; Fat mass; Lean mass; Low birth weight; Muscle mass.