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, Simonian & Herbison 1997 , Voisin et al. 1997 , Osterlund et al. 1998 , Merchenthaler et al. 2004 ). Recent evidence has shown that E2 has a nucleus-specific action in the hypothalamus to modulate energy homeostasis, particularly within the ARC and

Introduction The gonadal function is controlled by a complex interaction of regulatory signals, involving hypothalamus, pituitary and the gonads themselves. Altogether, they form the reproductive axis (a.k.a. the hypothalamic

hypothalamus have demonstrated that females have increased satiety-inducing pro-opiomelanocortin (POMC ARC ) neurons ( Nohara et al. 2011 ), reduced hunger-inducing neuropeptide Y (NPY) expression ( Urban et al. 1993 ), decreased sensitivity to central

later in life. Thus, the perinatal perturbation of foetus/neonate nutrient supply has been proposed to be a key determinant, especially the degree of mismatch between the pre- and post-natal environments ( Gluckman et al . 2008 ). The hypothalamus

Introduction The time at which puberty begins is the culmination of a series of events within the hypothalamus that results in the increased pulsatile release of luteinizing hormone-releasing hormone (LHRH) secretion. This change in LHRH

gonadotrophin, luteinising hormone (LH), then acts as an amplifier to the GnRH signal ( Clarke & Cummins 1982 ). In sheep, at least, the neurons that produce GnRH receive relatively little synaptic input compared to other neurons within the hypothalamus ( Lehman

studies have shown that leptin action is required for the formation of the axonal projections that extend from ARH neurons to important second-order neurons, such as the paraventricular nucleus of the hypothalamus (PVH) ( Bouret et al. 2004 a, b

those from citrate buffer (CB)-treated euglycemic fathers (CB-O). Our aim was to determine the impact of a paternal hyperglycemia on metabolic homeostasis of adult offspring, with particular focus on analysis of changes in hypothalamus-mediated food

regulation of food intake, as evidenced by increases in the expression of the anorexigenic neuropeptide corticotrophin-releasing factor ( Crf ) in the paraventricular nucleus of the hypothalamus (PVN) ( Uchoa et al. 2010 ) and reduction in the expression of

CNS, particularly the hypothalamus, plays a key role in modulating insulin sensitivity and energy homeostasis in vivo ( Knight et al. 2011 , Purkayastha et al. 2011 , Yang et al. 2012 ). Furthermore, changes in the levels of some nutrients