There has been significant progress in identifying genetic loci that affect normal pubertal timing, and the first single-gene causes of precocious and delayed puberty are being described. How these genes influence pubertal timing remains to be determined.
IntroductionThe neuropeptide kisspeptin sets the reproductive endocrine cascade in motion by stimulating the release of gonadotropin-releasing hormone (GnRH) from the hypothalamus (1). GnRH stimulates secretion of the gonadotropins follicle-stimulating hormone (FSH) and luteinizing hormone (LH) from the pituitary gland, and the gonadotropins in turn stimulate the release of sex steroids and other hormones from the gonads.The ability of kisspeptin to stimulate GnRH release allows it to be used as the first available probe of human GnRH neuronal activity. Our group and others have demonstrated that administering an intravenous bolus of kisspeptin to healthy men elicits an immediate pulse of LH secretion (2-4). Healthy women in the late follicular and luteal phases of the menstrual cycle similarly respond to kisspeptin with an LH pulse, though the response is attenuated in the early follicular phase (5-8).BACKGROUND. The neuropeptide kisspeptin stimulates luteinizing hormone (LH) secretion in healthy adults but not in adults with idiopathic hypogonadotropic hypogonadism. We hypothesized that, in children presenting with delayed or stalled puberty, kisspeptin would elicit LH secretion in those children found on detailed nighttime neuroendocrine profiling to have evidence of emerging reproductive endocrine function.
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