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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

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