wed, april 25

regulation of GH secreion: sim GH scc: GH affects metabolic pathways ... lobical that met factors ontreol GH
raised blood glucose stops secretion of GH and low blood gujlcoe raises SCC GH (short term/hours)
prolonged caloric deprivcation leads to raised GH (long term) probelmm that perons nom consuming sufficient protien rather than lower blood glucose levels (bf)
raised plasma AA (esp arginie) raises GH
acure stress raises GH (raised GH leads to raised glucose, and free fatty acid)
sleep leads to raised GH (GH has diuranl rhythm) inc sev hours after sleep

inhibition of GH:
low Th/hypotheyr.
raised corisol (classic strss hormoen) leads over time to raised cort low GH.
Emotional dep (bad emotional event)

Patterns of GH over life....
low from birth to childhood... goes up slightly in childhood and plattues until puberty.... spikes during puberty... and drops down to adulthood... and stays relatively stable after that....

GH no sig in prenatal growth (IGFs do
a+ at puberty, raises test and estrogens leads to GH secretion
estrgen acts directly on bone and everntually causes closeure of epiphyseal plate (cartilage)
in males, testo is converte to estrogen (closure)
test also acts dire on bone and dr stims growth (osteoblast activity)
estrogens alos stim bone growth
as people age greater than 60-70- GH declines and change in body comp lower muscle mass and raise percent fat.






disorders of GH secretion:
1) dwarfism - too little GH as a child

2) gigantism or giantism - too much
GH as a child

3) acromegaly - too much GH as an adult (pit tumor or hypoth. issue): increase in bone width, continued growth of cartilage, continued growth of soft tissues (liver, heart, tongue, kidneys), and tendency towards long standing hyperglycemia (diabetic over time)

Growth hormone mech of action...

this is the same for othes in the growth homrone family (prolactin)

one GH moelcue binds to two GH-R

JAK2 (just another kinase) is rebuited from the cytosol

JAK2 ginds to the GHR dimer and autophosphorylates on tyrosine residues (Y) (JAK2 is a tyrosine kinase)

JAK2 ph's the GHRs.

STATS (signal transducers and activators of transcription) bind to phos'd GHRs and are phos'd.

Two phos'd STATs are released into the cytoplasm and form a dimer and the dimer acts as a transcription factor to control gene expression.

(nothing to do with G protiens, no cAMP, etc)

GH circulates bound to a binding protein: extracellular doman of GH-R (aka GHR here )....
some GHR in liverare hydrolyzed and the extracellular domain leaves the plams membrane and is them GH-BP.

exam covers to here.....

Adrenal gland (medulla releases epi (E) and norepi (NE), is in the middle)(cortex surrounds medulla and releases steroid hormones)

E/NE are high in fight or flight sits. Cause heart rate to skyrocket during near miss.
they are secreted in response to stress.
but have other functions such as: regulate intermediary metabolism, regulate cardiovascular system, regulate secretion of other hormones.