Puberty and reproductive function are essential for the perpetuation of the species and, hence, are under the control of sophisticated regulatory networks, which integrate central and peripheral signals, as well as external cues. Among numerous regulators, puberty and fertility are highly sensitive to metabolic signals, and different metabolic stressors, ranging from subnutrition to morbid obesity, are known to have a discernible impact on the reproductive axis. In turn, gonadal factors substantially influence body weight and metabolism along the lifespan, acting at central and peripheral levels. While the neuro-endocrine substrate for such a close bidirectional relationship remains ill defined, our knowledge of the mechanisms whereby whole body metabolism and reproductive function are reciprocally controlled has recently expanded significantly. This has been due, to a large extent, to the discovery of the reproductive effects of leptin and other metabolic hormones (e.g., ghrelin, PYY3-36 or GLP-1), as well as the identification of the key reproductive roles of the neuropeptide, kisspeptin, that seemingly plays an important function as relay for the metabolic control of puberty and fertility at central levels. In this presentation, we will briefly summary these recent developments and will focus our attention on recent findings illustrating the roles of brain circuits involving cellular energy sensors, such as AMPK, and neuropeptide partners of kisspeptin, such as melanocortins, in the integral regulation of puberty, reproduction and body weight homeostasis.
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