male Flashcards
Factors Controlling sexual differentiation
The Male (XY) has the SRY gene and makes the SRY protein that develops the gonads into testes
The testes then make testosterone (and DHT) which cause the wolffian ducts to become the male reproductive tract and (DHT make the genitals male)
The testes then make antimullerian hormone (and the mullerian ducts regress(no female reproductive tract)
Male reproductive function from conception to death
- Fetal testes secrete antimullerian hormone that induces tregression of mullerian ducts, they also secrete androgents (T and DHT) that induces fetal differentiation into male phenotype. The burst in fetal testicular activity is stimulated by LH and FSH
- FSH and LH peak at 6 months post birth, to stimulate testosterone productions in the brain
- Puberty starts in the same way as females (GnRH pulses the increase of FSH and LH)-> sperm production and steroidogenesis. Pubertal increase in testicular androgen secretion induces the development of male secondary sex characteristics
- There is a decline in male reproductive function
Testicular steroidogenesis
- Local testosterone diffuses into seminiferous tubules
- Testosterone secreted into systemic circulation is carried by serum SHBG (sex hormone binding globulin)
- Testosterone can be converted into DHT (more potent androgen) by 5 alpha reductase or to estrogen by aromatase
Testicular, Adrenal and peripheral converstion of sex hormones
Testicular secretion (mostly testosterone, a little DHT and estradiol)
Adrenal secretion (mostly DHEA)
Peripheral conversion of precursors (mostly DHT, estrogens)
Men do have circulating estrogens (a little is produced by testes) aromatase is in peripheral tissues and will convert t to E (mostly in fat)
Mechanism of action of Testosterone
Plasma Testosterone dissociates from SHBG (and albumin)
and diffuses into the cytoplasm
There its converted into DHT by 5 alpha reductase
T can also bind to androgen receptor in nuclease (but DHT has a higher affinity)
Transcription and translation into proteins
Puberty
Pulsatile GnRH release from hypothalamus. (Men do produce prolactin to inhibit FSH AND LH) if you have a prolactin secreting tumor, you will inhibit FSH and LH and therefore inhibit T and DHT production from the testes
Testosterone induces an increase in growth hormone to stimulate linear growth (through IGF1) and has strong effects on spermatogensis
Major stimulator of spermatogenisis is FSH and local testosterone stimulation
Testosteron induces secondary sex charc. and testosterone will close the growth plates
LH and FSH go up together
Hormonal action on the testicular cells
LH stimulates leydig cells (like thecal cells in fem) and FSH stimulates sertoli cells (Like granulosa cell in fem)
The leydig cell produces testosteron which is released int the system and has androgenic effects and local effects to stimulate the sertoli cell (to make sperm). Testosterone exerts negative feedback effects (like E), but inhibin inhibits FSH
Process of spermatogensis
LH Stimulates leydig cells steroidogenisis (of T)
Testosterone/ DHT enters nuclease of Sertoli Cell
When sertoli cell is activated by FSH (and therefore cAMP and Protein kinase A)-> transcription and translation of proteins
Proteins are sperm growth factors
FSH+ testosteron (from leydig) also increases the production of ABP (local sink for testosterone in steady state its half unbound so it bathes the sperm in local free T)
Sertoli can also make inhibin and aromatase