Nutrition Bytes

With the current growing epidemic of obesity in the United States [18] and broad acceptance of the idea that the prenatal period may be a critical period for programming permanent changes in metabolic processes, increasing attention in the past decades has focused on the idea that intrauterine events can program adult obesity. Animal and human studies supporting a relationship between prenatal malnutrition and postnatal obesity [14,15] have spurred research elucidating mechanisms of prenatal programming of obesity. This paper reviews evidence for the role of leptin in programming of postnatal obesity by prenatal malnutrition based on published studies in animals and humans. Though human evidence is reasonably limited by the ethics of well-controlled trials studying fetal malnutrition, sufficient animal evidence exists to support several biologically-plausible mechanisms involving programming of leptin resistance at the level of the hypothalamus. Though more research is needed to provide conclusive data regarding the role of leptin in mediating the postnatal effects of prenatal malnutrition, evidence for mechanisms of prenatal programming of obesity may have widespread implications for public health and medicine in the future.