Male Puberty Flashcards
Describe the basic events that occur with the gonads during gestation
Early in gestation germ cell migration begins and sertoli and Leydig cells begin to be produced from a gonad. Sertoli cells form seminiferous tubes and secrete AMH to cause regression of Mullerian ducts, while Leydig cells are stimulated by placental hCG and secrete testosterone and INSL3. By week 11 all testicular components are present, sertoli cell masses continue to increase, and the testicles descend to the inguinal ring at 14 weeks and then to the scrotum at 35 weeks.
What is the minipuberty experienced by newborns?
There is a rapid rise in testosterone up to 400nd/dL in the first day of life that declines rapidly during the first week to 20-50, then increases over the first 2 months postnatally (this occurs due to transient activation of the HPG axis before CNS inhibition is fully mature). The levels then decline again to prepubertal levels by 1 yr.
During this minipuberty, FSH levels are higher than LH and penile length increases
What are some factors that suppress GnRH pulsatile release after the minipuberty until puberty?
- GnRH
- NPY
- GABA
- Leptin
- TGF-a
What is Kisspeptin?
A protein believed to be responsible for allowing pulsatile release of GnRH for the onset of puberty. This protein binds to GPR54 receptors on the GnRH neuron body to allow release from the axonal body.
Other stimulatory molecules include leptin, glutamate, and norepinephrine
T or F. GPR54 (the receptor for kisspeptin) is sensitive to GnRH antagonists
T. So it will be turned off as well
NOTE: GPR54 and kisspeptin have increased expression at the time of puberty (maximal expression)
Puberty is marked by the increase in the pulse frequency and amplitude of GnRH, increase in FSH and LH pulses, and rise in gonadal hormones
What neurotransmitters stimulate the HPG axis at the onset of puberty? Inhibit?
Stimulate- GlutamateInhibit- GABA
T or F. Changes in expression of tumor suppressor genes like Oct-2, EAP-1, TTF-1 are permissive for puberty onset
T.
What is Williams Sydrome?
Deletion of 7q11.23 results in normal onset of puberty with rapid progression (point: Genes contiguous with elastin affect pace of puberty)
Signaling through which parts of the hypothalamus are inhibitory to the onset of puberty? Stimulatory?
–Inhibitory tracts appear routed through the posterior hypothalamus
–Stimulatory tracts appear routed through the anterior hypothalamic preoptic area
What is Anosmia?
lack of normal sense of smell
What are some genes that when upregulated inhibit the release of GnRH and the onset of puberty?
–GnRHR
–KAL-1
–FGFR-1
–GPR54
–LHX3
What does mutation in KAL-1 cause?
Clinically, mutation results in the X-linked form of Kallmann syndrome. Individuals with Kallmann syndrome experience anosmia (lack of smell) and do not go through puberty (hypothalamic hypogonadotropic hypogonadism).
How is leptin involved in puberty control?
Leptin is secreted by fat cells and in addition to increasing insulin sesnitivity and satiety, acts on the hypothalamus to stimulate GnRH secretion. Thus, deficiency (commonly in very athletic young females with low body fat) can delay puberty. Similarly, prolonged excess of leptin in obese children down regulates GnRH release so delayed puberty can be seen in fat children as well