Puberty is considered to be a period of transition consisting of both physiological and morphological changes when an individual becomes a fecund adult from a juvenile. All mammals undergo puberty (1) although the precise timing of this event is different for each species. Pubertal onset, in mammals, is governed by the pulsatile release of gonadotropin-releasing hormone (GnRH) from the hypothalamus. GnRH promotes secretion of follicle-stimulating hormone (FSH) and luteinizing hormone (LH) from the pituitary gland which in turn stimulate the gonads. This process ultimately leads to the development of secondary sexual characteristics. The starting point for the hypothalamic-pituitary-gonadal (HPG) axis is GnRH and its secretion is controlled
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GnRH is released from the hypothalamus (see fig 1), passes via the portal system to the pituitary to stimulate the release of gonadotrophins from the adenohypophysis. In men LH stimulates the Leydig cells present in the testes to secrete testosterone whilst FSH binds to the Sertoli cells and promotes spermatogenesis. In women the LH leads to ovulation whilst FSH stimulates the Granulosa cells and initiates follicular growth. It is known (2) that the GnRH neurones migrate from the olfactory placode along the vomeronasal nerves. The factors that control this migration are not completely understood. One gene involved in the migration (3) of GnRH neurones is the KAL1, which encodes the protein anosmin-1. This gene is located on the x chromosome and is required for both olfactory receptor neurones and GnRH neurones to enter the brain. This gives rise to the symptoms of anosmia and hypogonadotropic hypogonadism. There are other mutations which affect GnRH neuronal migration. The fibroblast growth factor receptor 1, encoded by the FGFR1 (4) gene, is important in the development of olfactory receptors. Another example of a mutation in a gene causing failure of GnRH neuronal migration is with the NELF (5) gene that encoded for nasal embryonic LH-releasing hormone factor (NELF). NELF is needed for the attachment of GnRH neurones to the olfactory receptor axons. The GnRH neurones attach and …show more content…
Kisspeptin relatively seems to be much more important in GnRH secretion as it has been shown that there is a fourfold increase of mean LH concentrations when kisspeptin-54 has been administered. NKB as previously stated only causes modest rises of LH concentration in healthy volunteers and requires a comparatively high dose to elicit a significant LH response. The role of NKB, therefore, is much more nuanced as its absence (7,12) leads to hypogonadotropic hypogonadism. It is currently theorised that NKB acts on the GnRH neurones and its actions are dependent on the oestrogen status of the individual. This means that NKB modulates GnRH secretion rather than being a clear promoter or inhibitor of GnRH secretion. Finally, Young et al. (13) have shown that administration of kisspeptin in patients with inactivating mutations of TAC3 and TAC3R is able to restore LH pulsatility. This means that although NKB is important the role it plays it may not be as critical to pubertal onset as previously
GnRH is released from the hypothalamus (see fig 1), passes via the portal system to the pituitary to stimulate the release of gonadotrophins from the adenohypophysis. In men LH stimulates the Leydig cells present in the testes to secrete testosterone whilst FSH binds to the Sertoli cells and promotes spermatogenesis. In women the LH leads to ovulation whilst FSH stimulates the Granulosa cells and initiates follicular growth. It is known (2) that the GnRH neurones migrate from the olfactory placode along the vomeronasal nerves. The factors that control this migration are not completely understood. One gene involved in the migration (3) of GnRH neurones is the KAL1, which encodes the protein anosmin-1. This gene is located on the x chromosome and is required for both olfactory receptor neurones and GnRH neurones to enter the brain. This gives rise to the symptoms of anosmia and hypogonadotropic hypogonadism. There are other mutations which affect GnRH neuronal migration. The fibroblast growth factor receptor 1, encoded by the FGFR1 (4) gene, is important in the development of olfactory receptors. Another example of a mutation in a gene causing failure of GnRH neuronal migration is with the NELF (5) gene that encoded for nasal embryonic LH-releasing hormone factor (NELF). NELF is needed for the attachment of GnRH neurones to the olfactory receptor axons. The GnRH neurones attach and …show more content…
Kisspeptin relatively seems to be much more important in GnRH secretion as it has been shown that there is a fourfold increase of mean LH concentrations when kisspeptin-54 has been administered. NKB as previously stated only causes modest rises of LH concentration in healthy volunteers and requires a comparatively high dose to elicit a significant LH response. The role of NKB, therefore, is much more nuanced as its absence (7,12) leads to hypogonadotropic hypogonadism. It is currently theorised that NKB acts on the GnRH neurones and its actions are dependent on the oestrogen status of the individual. This means that NKB modulates GnRH secretion rather than being a clear promoter or inhibitor of GnRH secretion. Finally, Young et al. (13) have shown that administration of kisspeptin in patients with inactivating mutations of TAC3 and TAC3R is able to restore LH pulsatility. This means that although NKB is important the role it plays it may not be as critical to pubertal onset as previously