Prenatal influences on susceptibility to diet-induced obesity are e

prenatal undernutrition and postnatal high-fat nutrition on key genes of the hypothalamic appetite regulatory network. OBRb gene expression together with elevations in circulating levels of both plasma leptin and insulin. These findings are have important consequences on metabolic energy regulatory systems in later life (Barker & Osmond 1986, Ravelli et al. induce long-term effects on behavioural, anthropometric and cytoplasmic region that is required for signal transduction. Moreover, evidence is accumulating to suggest that obesity is homeostasis. 31Journal of Endocrinology (2007) 193, 31–37metabolic functions (Freinkel 1980, Lucas 1991). Since the developing fetus is sensitive to environmental conditions that Key targets of leptin action are the orexigenic neurons within the hypothalamic arcuate nucleus that co-express the DOI: 10.1677/joe.1.070171999, Vickers et al. 2000). Much of our current knowledge of the importance of prenatal nutrition has been derived from animal studies. In the rodent, the impact of maternal nutrition has been shown to associated with central leptin resistance (Flier 2004). For this reason, investigations over the past decade have focused on determining the mechanisms involved in the action of leptin on hypothalamic neural circuitry systems involved in energyepidemiological, clinical and experimental studies suggest that the nutritional environment during the prenatal period may tissues. Five alternatively spliced forms of the leptin receptor are produced (OBRa–e), of which only OBRb has a longlibitum (AD) or at 30 % of AD intake throughout gestation (UN). From weaning, female AD and UN offspring were fed either a standard chow (ADC nZ8, UNC nZ8) or a high-fat diet (45 % kcal as fat; ADHF nZ8, UNHF nZ8) ad libitum for the remainder of the study. At 24 weeks of age, body composition was assessed by dual energy X-ra