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87 Cards in this Set

  • Front
  • Back
classification of adenohypophyseal hormones
somato-lactogen group
two-subunit group
proopiomelanocortin
somato-lactogen group
prolactin/leuteotropin
growth hormone/somatotropin

placental lactogen
placental lactogen
not a pituitary hormone but structurally similar to PRL & GH

synthesized in placenta only during pregnancy
two-subunit group
leuteinizing hormone
follicle stimulating hormone
thyroid stimulating hormone
proopiomelanocortin
large precursor protein broken down into ACTH
chemistry of GH
190 aas
20 kDA = effectively filtered by the kidneys
4 a-helices
hypothalamic control of GH
mediated by regulation of cyclic-AMP at median eminence

GH-RH
GH-RIH/somatostatin
negative feedback regulation of GH

inhibition of GH-RH
increased blood GH levels

IGF-I inhibits GH-RH and stimulated GH-RIH
physiological down regulation of GH
glucose

stress
physiological up regulation of GH
aas
exercise
sleep
ADH
ghrelin ( secreted from gut after meal )
Transportation of GH in plasma
released in short bursts, bind to carrier protein to stabilize conc of GH according to equilibrium

only free GH is released from blood
GH Mechanism of Action
1)direct effects on target tissues

2)indirect effects on target tissues
GH direct effects on target tissues
stimulated target tissues synthesize and release IGF-I

liver-synthesized IGF-I acts on pituitary gland in negative feedback loop
GH indirect effects on target tissues
via IGF-I produced by direct target tissues

ie. bone growth
GH biochemical mechanism of action
GH binds two plasma membrane GH-receptors activing the JAK/STAT pathway

regulates expression of GH-specific genes
biological actions of growth hormone

ie. What does Growth Hormone do to the body?
effects on:
bone growth
carbohydrate metabolism
lipid metabolism
protein metabolism
mammary gland matabolism
growth hormone effects on bone growth
classically mediated by IGF-I
growth hormone effects on protein metabolism
growth hormone promotes uptake and synthesis of proteins

"protein-sparing" effect

increased protein = increased nitrogen content
growth hormone effects on carbohydrate metabolism
glucose-sparing, antagonizing the use and uptake of glucose
growth hormone effect on lipid metabolism
releases lipid from adipocytes to be metabolized
growth hormone effects on mammary gland metabolism
auguments/stimulates lactation
indirectly mediated by IGF-I

BST= recombinant bovine somatotropin given to dairy herds, controversial
chemistry of prolactin
200 aas
22 kDa
similar structure to GH, 4 a-helices
placental prolactin
produced by placenta only during pregnancy

shuts down pituitary production of PRL
pituitary synthesis of PRL
majority of synthesis of PRL

other sources are not significant contributors
hypothalamic regulation of PRL
dopamine "prolactin release-inhibiting hormone"

thyrotropin-releasing hormone
effect of dopamine on PRL production
"brake" or suppress

PRL in constant state of suppression via Prolactin Release-Inhibiting Hormone
effect of thyrotropin-releasing hormone on PRL production
"accelerator" or simulator
feedback regulation of PRL
PRL inhibits synthesis

acting on hypothalamus and adenohypophysis
physiological regulation of PRL
steroids

suckling response

pregnancy
effect of steroids on PRL production
estrogen stimulates pituitary synthesis & secretion considerably
effect of suckling response on PRL production
stimulates brain to increase prolactin levels

increases amount of food for baby and maintain breast function
effect of pregnancy on PRL production
placental prolacting feedbacks to hypothalamus and adenohyphophysis to suppress pituitary prolactin production
transportion of PRL in blood
no carrier protein

low circulating levels in males, higher in females

highest during pregnancy and lactation
PRL mechanism of action
binds a pair of prolactin-receptors at plasma membrane, activating JAK/STAT pathways

increase in prolactin gene expression
biological actions of prolactin
mammary growth and lactation
rodent corpus luteum
male reproductive system
effect of PRL on mammary growth and lactation
stimulate initiation of lactation

stimulate maintenance of lactation in some species
effect of PRL on rodent corpus luteum
stimulates corpus luteum to produce progesterone

"luteotropic hormone"
effect of PRL on male reproductive system
maintains accessory sex glands
effect of PRL in birds
maintains crop sac biology

crop: where crop milk is made
effect of PRL in fish
high concentration of PRL-receptors in fish kdiney cell membranes

alters function of kidney when transitioning between fresh and salt water to adjust to new saltity
placental lactogens
species specific

biological activities more similar to GH in some species and PRL in other species

NOT a pituitary hormones; produced by placenta during pregnancy
chemistry of thyroid stimulating hormone
a-subunit = 89aa
b-subunit = 112 aas
29 kDa glycoprotein
1% sialic acid
hypothalamic control of TSH
thyrotropin-releasing hormone

somatostatin
effect of thyrotropin-releasing hormone on thyroid stimulating hormone production
acts from hypothalamus on adenohypophysis to increase production and secretion of thyroid-stimulating hormone

(also stimulates PRL release)
effect of somatostatin on thyroid stimulating hormone production
decreases TSH release from adenohypophysis

(also decreases GH release)
feedback regulation of TSH
T3 & T4 act on hypothalamus to diminish TRH production, thus diminishing TSH production
physiological up regulation of TSH
cold stress
estrogens
physiological down regulation of TSH
glucocorticoids
GH
transportation of TSH in blood
NO carrier protein

half life = 75 min
TSH mechanism of action
binds 1 plasma membrane receptor, activing G-protein, which activates adenylate cyclase
ATP converts it to cyclic-AMP, activing a protein kinase to modulate TSH gene expression
biological effects of TSH
stimulate synthesis and secretion of thyroid hormones (multi-step process)
chemistry of FSH
a-subunit = 89 aas
b-subunit = 115 aas
29 kDa glycoprotein
5% sialic acid (longer 1/2 life)
hypothalamic control of FSH
gondadotropin releasing hormone (GnRH)
effect of inhibin on FSH production
produced by gonadal tissues in both males and females for the purpose of reducing pituitary response to gonadotropin-releasing hormone
effect of estrogen on FSH production
in females, can stimulate or depress FSH secretion via hypothalamus
physiological regulation of FSH
closely regulated by neural input:

females: cyclic activity
males: noncyclic activity
transport of FSH in blood
NO carrier protein

half life = 3 - 4 hours
FSH mechanism of action
bind and activate FSH-receptor, activating G-protein, stimulating ATP conversion of adenylate cyclase into cyclic-AMP, stimulating a protein kinase and gene transcriptions
biological effect of FSH
effects on ovary

effects on testis
effect of FSH on ovaries
stimualate development of primary follicle
effect of FSH on testis
stimulate spermatogenesis and growth of the seminiferous tubules

stimulates production of angroden-binding protein from sertoli cells
feedback regulation of FSH
inhibin

estrogen
chemistry of luteinizing hormone
29 kDa
a-subunit = 89 aas
b-subunit = 115 aas
1% sialic acid (shorter 1/2 life)
hypothalamic control of LH
gonadotropin-releasing hormone (GnRH)
molecules which feedback regulate LH in males
testerone inhibits LH secretion
molecules which feedback regulate LH in females
during follicular phase:
estrogen stimulates LH secretion

during luteal phase:
estrogen and progesterone inhibit LH secretion
physiological regulation of LH
neural inputs
(temp, light, environment, etc.)

cyclic in females
noncyclic in males
transportation of LH in blood
no carrier protein

cyclic range in females can be an order of magnitude
how does LH act on cell?
binds and activates LH-receptor, activing G protein, stimulating conversion of adenylate cyclase in cyclic-AMP by ATP, stimulating protein kinases, controlling gene transcription
effects of luteinizing hormone on ovary
1) corpus luteum development

2)progesterone synthesis and secretion by corpus luteum
effects of luteinizing hormone on testis
stimulate testosterone synthesis and secretion
non-pituitary gonadotropins
pregnant mare serum gonadotropin

human chorionic gonadotropin
proopiomelanocortin is a precursor for...
ACTH

MSH

LPH
chemistry of POMC
29 kDa
chemistry of ACTH
31 aas
chemistry of MSH
13 aas

cleaved in pars intermedia
chemistry of Beta Lipotropin (LPH)
91 aas
hypothalamic regulation of POMC
corticotropin-releasing hormone (CRH)

melanocyte-stimulating hormone-releasing factor (MSH-RF)

melanocyte-stimulating hormone release-inhibiting hormone
feedback regulation of POMC
ACTH stimulates adrenal steroids

adrenal steroids feedback regulate hypothalamus to dec. CRH production

adrenal steroids feedback regulate adenohypophysis to dec. ACTH production
physiologic regulation of POMC
neural input

ie. stress, cold exposure, pain, emotion, diurnal cycle, hemorrhage, exercise, hypoglycemia, infection, trauma, toxins, etc.
transport of ACTH in blood
no carrier protein

half life = 6-9 min
therefore, released in bursts

easily filtered by kidneys b/c so small
ACTH mechanism of action
ACTH-bound receptor activates G protein, stimulating c-AMP,

activing side chain cleavage enzyme,
converting cholesterol to pregnenolone
MSH mechanism of action
MEESH-bound receptor activates G protein, activing c-AMP

activates side chain cleavage enzyme
converts cholesterol to pregnenolone
biological actions of POMC molecules
ACTH acts on adrenal gland

B-LPH acts on adipose tissue

MSH acts on melanocytes
effect of ACTH on adrenal gland
stimulates synthesis and secretion of glucocorticoids

glucocorticoids are at highest concentration around time of wakening and bottom out at 3-4 PM in nonnoctural species
effects of beta lipotropin hormone on adipose tissues
stimulates lipolysis from triglycerides
effect of MSH on melanocytes
stimulates melanocytes in skin to synthesis and secrete pigment