Reproduction Abstracts

The adipose hormone, leptin, which was identified in 1994, has been universally recognized as an essential metabolic signal that transmits information about the magnitude of body energy reserves to the brain centers controlling body weight homeostasis and energy expenditure. In addition, leptin serves a fundamental function as integrator of metabolism and other key bodily systems, ranging from immune responses to the reproductive axis. On the latter, leptin is known to metabolically gate reproductive activation at puberty and fertility, acting mainly as a permissive factor; namely, threshold leptin levels are needed for puberty to proceed and for the maintenance of reproductive competence. However, we have become aware in recent years that the mode of action of leptin for its effects on the reproductive axis is multi-faceted, and includes permissive and inhibitory actions, involving numerous pathways, at different levels of the hypothalamic-pituitary-gonadal system. In this talk, we will present a summary of recent advancements in our knowledge about the mechanisms whereby leptin transmits metabolic information to the reproductive axis, with special attention to its mode of direct or indirect regulation of various brain neuropeptide systems, including kisspeptins, neurokinin B and melanocortins, as well as the central roles of key cellular energy sensors. In doing so, we aim to provide an updated view of the mechanism of action of this essential physiological and pathophysiological regulator of puberty and fertility.