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26 Cards in this Set

  • Front
  • Back
endocrinology
study of hormones, receptors, and the intracellular signaling pathways they stimulate
hormone usually stimulates ___ cells
target (specific); travel via blood
types of hormonal communication
endocrine (travel long distance thru blood --> traget); paracrine - local action, diffuse to neighboring target cells (ex testost from lytic cells --> affect sertoli cells or granulosa cells from estrogen); autocrine - acts on same cell (self, often case w/ reproductive cancer)
hormone agonists
(often natural), bind to receptor + stimulate post-receptor events that lead to bio effect - can have dif potencies
hormone antagonist
bind to receptor + repress activation by hormone or agonist + fail to trigger intracellular signaling events (used to halt cancers)
# receptors per cell
1,000- 10,000 recep molecs per cell but only 10^-9 M hormone concentration in blood
dif b/w production of peptide and steroid hormones
peptide hormones translated from RNA; steroid hormones = lipids made from cholesterol by series of enzymatic rxns
conventional numbering and lettering of steroids goes:
from bottom left to top right
3 domains of nuclear receptors
variable - "functional", changes in AA and composition based on the receptor, job is to bind to accessory proteins used in transcription (like RNA polym + coactivators/repressors); DNA-binding - highly conserved - binds to HRE (Hormone Response Elements) = specific regions on DNA (can be ARE = androgen response or ERE = estrogen response); Steroid-binding - steroid specific
can steroid hormone receptors act w/o hormone?
yes! some bind to HRE (hormone response elements - ex androgen or estrogen response elems) and repress transcrip in absence of hormone, others use chems (enviro,drugs,etc) to activate or repress activity of receptor and modify hormone-regulated gene trasncription
what are natural bodily sources of estrogen?
from uterus or from testosterone converted via adipose fat (esp in breast)
discuss tamoxifen
anti-estrogenic in breast but estrogenic in uterine walls (can cause uterine cancer)
what does SERMS stand for?
selective estrogen receptor modulators
how do progestins and antiprogestins avoid pregnancy?
progestins inhib LH surge + ovulation. antiprogestins can stim abortion by inhibiting activity of progesterone to maintain uterine lining
what is androgen insensitivity syndrome?
result of androgen receptor gene mutation - inability to respond to testosterone (androgen = male steroid hormone) that body produces - ex. even with Sry gene have testis (undescended) + breasts but no underarm hair, descended testes, scrotum b/c these happen in response to androgens
domains of peptide hormone receptors
extracellular (bind to peptide hormone); intracellular (bind to cytoplasmic proteins involved in signaling pathways); transmembrane (position receptor in lipid bilayer)
G-proteins
closely coupled to receptors (initiate signal transduction cascade)
types of 2ndary messengers
cAMP, IP3, DAG, Ca2+
LH and FSH receptors localized to steroidogenic cells in gonads such as..
Leydig cells in testis, granulosa in ovaries
7-transmembrane receptor also known as
G-protein coupled receptor
True/False G-proteins always activate adenylate cyclase + therefore cAMP production
false - depends on which G protein
how is a G-protein's activity initiated?
by turning GDP --> GTP and activating adenylate cyclase to make cAMP by cleaving ATP --> kinase's activity (GDP eventually regenerated)
how does Viagra work?
cGMP (like cAMP) increases blood flow to penis so viagra inhibs enzyme that degrades cGMP
explain gonadatropin signal transduction cascade
once LH and FSH are in blood, act on receptors --> stim adenylate cyclase --> make cAMP --> stim Protein Kinase A
explain GnRH intracellular signal transduction cascade
end goal: GnRH stims release of gonadatropins LH and FSH: GnRH attaches to receptor on gonadatrophs in ant pituitary --> activates phospholipase C --> produces secondary messengers IP3 and DAG --> DAG stimulates protein keinase C and IP3 stimulates release of Ca+ into cytoplasm which --> stims release of LH and FSH by exocytosis into blood
clinical examples of peptide hormone-related pathology
hypogonadotropic and/or hypogonadal = infertility; precocious puberty = too much steroid hormone (in males due to testototoxosis from too much cAMP --> too much Leydig activiation --> too much testost) hastens bone growth + aging so epiphyseal plate seals + adult height stunted