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53 terms

endo5

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5 cell populations of anterior pituitary (and what they secrete)
corticotrope (ACTH), thryotrope (TSH), gonadotrope (FSH & LH), somatotrope (GH), lactotrope (PRL)
somatotrope cells (size) secrete (what secretion regulates - general)
large - GH - regulates linear growth
lactotrope cells (size) secrete (what secretion regulates - general)
large - PRL - regulates lactation
corticotrope cells (size) secrete (what secretion regulates - general)
small - ACTH - regulate adrenal function
thyrotrope cells (size) secrete (what secretion regulates - general)
large - TSH - regulate thyroid gland function
gonadotrope cells (size) secrete (what secretion regulates - general)
large - LH (regulate corpus luteum formation, estrogen/progesterone secretion & androgen secretion) & FSH (regulate growth of ovarian follicles and spermatogenesis)
small vs. large proteins, what it means
small have specific targets and large have general targets
three proteins that are glycoproteins and form dimers
TSH, LH, FSH
GH and PRL have what in common
come from same family/have common ancestor
GH regulates
growth and metabolism
how does GH circulate
bound to GH binding proteins
most abundent cell type in pituitary
somatotrophs (make GH)
somatostatin
GH inhibitor (IH) - only example of hypothalamus producing an inhibitor
GRH
GH enhancer (RH) - promotes somatotrope cell proliferation - thus GH secretion
GHS (name and function)
GH secretagogue - a small synthetic molecule receptor that has the same function as GRF - promotes GH secretion.
central control factors of GH
GRF (GHRH), somatostatin (SST), GHS, catecholamines (NT)
neurotransmitter system of GH secretion
catecholamines bind to either alpha or beta adrendergic receptors and modulate GHRH and somatostatin output
alpha-adrenergic receptor
stimulates GH secretion with the binding of catecholamines
beta-adrenergic receptor
suppressess GR secretion with the binding of catecholamines
peripheral control factors of GH secretion
Ghrelin, glucocorticoids, thyroid hormone, gonadal steroids (estrogen, androgens), leptin
ghrelin
hormone that causes GH release - activates GHS (subsequent cAMP increase and Ca release)
glucocorticoids (peripheral GH secretion control)
dual effect - first they stimulate secretion, then they can inhibit.
4 peripheral controls of GH secretion that only stimulate GH secretion
thyroid hormone, gonadal steroids, leptin, and ghrelin
indirect controls of GH secretion
glucose levels, amino acids, nonesterified fatty acids, excercise/stress
glucose (indirect control of GH)
glucose inhibits GH secretion (hypoglycemis stimulates GH secretion)
amino acids (indirect control of GH)
certain amino acids are potent inducers of GH secretion
nonesterified fatty acids (indirect control of GH)
reduce GH secretion
exercise and stress (indirect control of GH)
stimulants of GH secretion
Growth hormone receptor activates
Jak/Stat pathway
IGFs
insulin-like growth factors - relate to body size (the more the IGF, the larger the body size) but does not correlate to GH secretory capacity
IGF cascade
GH - liver - IGFs - growth
how do IGFs circulate
bound to IGF binding proteins
IGF I
growth factor at all stages
IGF II
fetal growth factor
Type I IGF receptor
major signaling receptor
type II IGF receptor
may function to destroy excess IGF II in fetus
hypopituitarism
GH associated disease - pituitary hormone dificiency caused by diseases (ex. tumors)
McCune-Albright Syndrome
GH associated disease - mutation of g-protein causes decreased GTPase activity. - constitutive AC activity
pituitary dwarfism
GH associated disease - GH deficiency (tumors, genetic defects, etc)
laron dwarfism
GH associated disease - GH resistence caused by GH receptor defects (worse than pituitarty dwarfism) - depressed IGF I levels
gigantism
GH associated disease - excess GH early in life - symmetrical enlargement - often a pituitary tumor secreting GH
acromegaly
GH associated disease - excess GH in adults - asymmetrical enlargement
gigantism and acromegaly both caused by
tumors made up of somatotroph cells that are leading to excess GH at different times (early life/adulthood)
how GH deficiency has been treated
past - pituitarty extracts from cadavers. now - recombinant GH protein
STAT5 mutation
leads to GH inesnsitivity
how is GH secreted
pulsatile fashion - every 2-3 hours (ultradian)
general biological factors that affect GH secretion
sex (women more than men), age (birth-elevated for a few days, puberty - increases alot, adulthood - stable thru 5th decade, aging - after this point it starts to decrease), *sleep (most prominent GH release occurs during onset of deep sleep)
during sleep - GH secretion
increases during onset of deep sleep, 3 pulses around midnight
positive and negative controllers of GH
+ = GRF & - = somatostatin
introduction of insulin results in
hypoglycemia, thus an inc. in GH production
GHR
growth hormone receptor - activates Jak/Stat pathway
if you knockout IGF I
slow growth in utero and after birth
if you knockout IGF II
slow growth in utero, but will grow fine after birth