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خرید پکیج
تعداد آیتم قابل مشاهده باقیمانده : -8 مورد

Hypothalamic-pituitary-testicular axis and puberty

Hypothalamic-pituitary-testicular axis and puberty
Puberty is marked by an increase in the pulsatile secretion of GnRH from the hypothalamus.[1] GnRH stimulates the secretion of FSH and LH from the gonadotroph cells of the anterior pituitary gland. In children assigned male at birth, FSH stimulates growth of seminiferous tubules, leading to an increase in testicular volume. FSH also stimulates the Sertoli cells of the testes to produce inhibin, which inhibits secretion of FSH. LH stimulates the Leydig cells of the testes to produce testosterone, which induces growth of the penis, deepening of the voice, growth of facial and body hair, and increases in muscularity. The high local concentration of testosterone in the testes further stimulates growth of the seminiferous tubules. Some testosterone is converted to estradiol, which stimulates growth and skeletal maturation and frequently leads to some breast development (gynecomastia).

FSH: follicle-stimulating hormone; GnRH: gonadotropin-releasing hormone; KNDy: kisspeptin-neurokinin B-dynorphin; LH: luteinizing hormone; MKRN3: makorin RING-finger protein 3; NKB: neurokinin B.

* The site of action of MKRN3 within the hypothalamus is unknown. One possibility is that MKRN3 may work within KNDy neurons to inhibit puberty initiation by suppressing transcription of the genes that encode kisspeptin and NKB[2].

¶ It is uncertain whether NKB acts on the KNDy neurons, GnRH neurons, or both and whether these are the primary sites of action. NKB appears to be important for pubertal timing but does not appear to be an obligate part of the hypothalamic-pituitary-gonadal axis, as there can be reproductive endocrine activity in the absence of NKB[3].
References:
  1. Hughes IA. Releasing the brake on puberty. N Engl J Med 2013; 368:2513.
  2. Abreu AP, Toro CA, Song YB, et al. MKRN3 inhibits the reproductive axis through actions in kisspeptin-expressing neurons. J Clin Invest 2020; 130:4486.
  3. Gianetti E, Tusset C, Noel SD, et al. TAC3/TACR3 mutations reveal preferential activation of gonadotropin-releasing hormone release by neurokinin B in neonatal life followed by reversal in adulthood. J Clin Endocrinol Metab 2010; 95:2857.
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