Abstract
Prenatal nutritional conditions exert fetal programming effects on offspring predisposing them to altered energy homeostasis later in life. Human epidemiological studies show that prenatal undernutrition or overnutrition increases the risk for developing obesity and type 2 diabetes mellitus in adulthood and, as such, bolster the Developmental Origins of Health and Diseases (DOHaD) hypothesis. Many animal models have confirmed that suboptimal maternal nutritional conditions are associated with altered birthweight and abnormal postnatal metabolic status. The mechanisms behind fetal programming, however, are poorly understood. The hypothalamus is critical in long-term regulation of body weight and energy homeostasis and has been proposed as a target site of fetal programming. This chapter presents evidence that changes in hypothalamic gene expression and neuronal connections underlie fetal programming observed after exposure to abnormal prenatal nutritional conditions.
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