Abstract
Puberty is a fundamental developmental event in the lifespan of any individual, when
sexual and somatic maturation is completed, and reproductive capacity is achieved.
While the tempo of puberty is under strong genetic determination, it is also modulated
by a wide array of internal and environmental cues, including, prominently, nutritional
and metabolic signals. In the last decade, our understanding of the neurohormonal
basis of normal puberty and its perturbations has enlarged considerably. This is illustrated
by the elucidation of the essential roles of kisspeptins, encoded by the Kiss1 gene,
in the hypothalamic circuits controlling puberty. Moreover, other neuropeptide pathways,
convergent with kisspeptin signaling, have been pointed out as important coregulators
of pubertal timing. These include the cotransmitters of Kiss1 neurons in the arcuate
nucleus (ARC), neurokinin B, and dynorphin, as well as melanocortins, produced by
ARC neurons expressing proopiomelanocortin, which are endowed with key roles also
in the control of metabolic homeostasis. This neuropeptide setup seemingly participates,
in a coordinated manner, in transmitting the regulatory actions of metabolic cues
on pubertal maturation. In this function, cellular metabolic sensors, such as the
AMP-activated protein kinase, and the fuel-sensing deacetylase, SIRT1, have also been
shown recently to contribute to the metabolic regulation of puberty. Altogether, elucidation
of the physiological roles of these signals and regulatory circuits will help uncover
the intimacies of the brain control of puberty, and its alterations in conditions
of metabolic stress, ranging from subnutrition to obesity.
Keywords
puberty - kiss1 - kisspeptins - GnRH - NKB - dynorphin - KNDy - melanocortins - obesity
