Increasing evidence indicates that early metabolic programming contributes to escalating obesity rates in children and adults. Metabolic imprinting is involved in the establishment of set points for physiologic and metabolic responses in adulthood. Evidence from epidemiological studies and animal models indicates that maternal health and nutritional status during gestation and lactation have long-term effects on central and peripheral systems that regulate energy balance in the developing offspring. Perinatal nutrition also impacts susceptibility to developing metabolic disorders and plays a role in programming body weight set points. The states of maternal energy status and health that are implicated in predisposing offspring to increased risk of developing obesity include maternal overnutrition, diabetes, and undernutrition. This chapter discusses the evidence from epidemiologic studies and animal models that each of these states of maternal energy status results in metabolic imprinting of obesity in offspring. Also, the potential molecular mediators of metabolic imprinting of obesity by maternal energy status including glucose, insulin, leptin, inflammatory cytokines and epigenetic mechanisms are considered.
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