The Association of Fetal Malnutrition with Metabolic Syndrome in Adulthood

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The purpose of the present study was to investigate a possible mechanism of developmental origins of metabolic syndrome.We developed a mouse animal model of fetal undernutrition (UN offspring) by maternal food restriction. The UN offspring developed an acceleration of obesity on high fat diet, dyslipidemia, impaired glucose tolerance and blood pressure increase in adulthood. In the UN offspring, we reveled a premature onset of leptin surge during neonatal period, which programmed permanent low leptin sensitivity in the hypothalamic energy regulation, concomitant with structural changes of hypothalamic neuronal circuit, such as neuropeptide Y (NPY) and cocaine and amphetamine regulated transcript (CART), contributing to an acceleration of obesity on high fat diet as well as impaired glucose metabolism (Yura S, Itoh H et al., Cell Metab, 2005,1,371).Thus, we here demonstrated that premature leptin surge during neonatal period plays a pivotal role in the developmental origins of obesity and associated detrimental metabolic disorders.