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Reproduksi
Hypothalamus/
Pituitary/Reproductive Organ Axis
Mekanisme
Steroid hormones penetrate the plasma
membrane and bind to intracellular
receptors in the nucleus or cytoplasm.
Hormone binding activates the
receptor, hormone response elements,
HRE on DNA to initiate transcription
and formation of the proteins that
express the hormonal response.
Reseptor Steroid
Membrane receptors that interact with kinases.
estradiol (E2) binds to an intracellular receptor
protein (ER) that dimerizes and translocates to the
nucleus
Estradiol also affects ion channels and G-proteincoupled receptors, independent of the ER nuclear
transcription factors
receptor complex, made of the receptor protein
and coactivators, binds to the palindromic
sequences (GCTAATCG) that constitute the
estrogen response element (ERE) and affect
gene transcription
Steroid
Cholesterol
Steroid
Cortex Adrenal : Steroid
Cortisol
Androgen
Laki-laki: Testosteron
Wanita : Estrogen dan progesteron
Male
Testis
Sel Leydig :androstenediol, androstenedione,
testosterone, dihydrotestosterone, dan
dehydroepiandrosterone (DHEA)
Sel Sertoli: merubah testosterone menjadi
estrogen (<); estradiol(E2)
(spermatogenesis).
FSH dan LH: proliferation Leydig cells
LH upregulates 3-hydroxysteroid
dehydrogenase, (last step in testosterone
formation)
Testis
Testis.
Testicular androgens : mostly produced
by the Leydig cells under the influence
of pituitary luteinizing hormone (LH).
Sertoli cells: sperm proliferation and
maturation and convert androgens to
estrogens via aromatase
Dihydrotestosterone via 5-reductase
secrete inhibin to regulate LH release
FSH- LH
FSH & LH: glycoprotein
hormones,synthesized and secreted by a
single class of pituitary cells
LH: Leydig cells
Receptors: heterotrimeric G-proteins (cyclic
AMP )
activates protein kinase A, promote
steroidogenesis, gene transcription, and other
cellular functions
Dihydrotestosterone (DHT)
Aromatase
Adipose tissue is an important source
of the enzyme aromatase that
converts androgens to estrogen.
Metabolisme testosteron
Female
Biosintesis estrogen
Biosintesis estrogen
three hydroxylation
steps, each of which
requires O2 and
NADPH.
The aromatase
enzyme complex :
P450
monooxygenase
FSH & LH
Ovari: control the menstrual cycle.
FSH : ovarian granulosa cell proliferation and
aromatase activity to allow production of E2.
E2 increases, FSH stimulates increased LH
responsiveness.
E2 and inhibin suppress FSH production at the level
of the hypothalamus and pituitary
release of a selected oocyte from th ovary (ovulation)
and transformation of granulosa cells into the
secretory luteinized cells of the corpus luteum.
Luteal cells make large amounts of P4, but also E2
and inhibin
FSH-LH
pregnancy does not occur : LH, sufficient to
support the corpus luteum (for very long).
P4, E2, and inhibin levels drop, FSH levels
rise. Menstruation begins and the cycle
repeats.
pregnancy, luteal P4 supports the pregnancy
until hormonal support is taken over by the
placenta (typically 79 weeks of gestation).
ovarian E2 and P4 directs the growth and
differentiation of the uterine endometrium
to prepare it for embryo implantation.
Prolactin & GH
Prolactin : controls the initiation of lactation. In
contrast to other pituitary hormones, it is not
negatively regulated by classic feedback loops but
rather by
local autocrine and paracrine factors
Neurotransmitters
peripherally produced steroid hormones.
Ovarian E2 and pituitary TRH are strong stimuli for prolactin
production.
Granulosa
express ample aromatase, but cannot produce its 19
carbon substrate because they lack P450c17.
However, granulosa cells readily aromatize androgens
provided by diffusion from the theca interna.
Menopause
Cessation of ovarian follicular development with resultant
marked decreases in circulating estrogen, inhibin, and
P4 levels.
Ovarian androgen production remains relatively intact.
Decreased estrogen and inhibin release, consequently
FSH levels rise.
hot fl ashes, insomnia, and depressed mood that are commonly
found in periand early postmenopausal women.
Estrogen deficiency: tissue atrophy and loss of elasticity in the
breast, vagina, and skin.
OXYTOCIN
Oxytocin: uterus to contract
and causes the cervix to
stretch.
Oxytocin secreted in response
to suckling.