Endocrine Abstracts

Reproduction is an energy-demanding function. Accordingly, acquisition of reproductive capacity at puberty is metabolically gated, as a means to prevent fertility in conditions of energy insufficiency. In addition, obesity has been shown to impact the timing of puberty and may be among the causes for the earlier trends of pubertal age reported in various countries, especially in girls but probably also in boys. The metabolic control of puberty in such a spectrum of situations, ranging from energy deficit to extreme overweight, is the result of the concerted action of different peripheral hormones and central transmitters that allow the sensing of the metabolic state of the organism and transmit this information to the various elements of the reproductive brain, mainly the GnRH neurons. In this presentation, we will provide a synoptic overview of recent developments that have deepened our understanding of the neuroendocrine and molecular basis for the metabolic control of puberty onset. These include not only the demonstration of the involvement of the hypothalamic Kiss1 system in the control of puberty and its modulation by metabolic cues, but also the identification of the roles of additional transmitters, such as neurokinin-B and nesfatin-1, and hypothalamic pathways, such as those originating from the ventral pre-mammilary nucleus, in the metabolic regulation of puberty. In addition, recent progress in the identification of putative molecular mediators for the metabolic gating of puberty will be reviewed here. All in all, characterization of these novel players and regulatory mechanisms will improve our understanding of the basis of normal puberty, and its eventual alterations in conditions of metabolic stress, ranging from anorexia to morbid obesity.