groth hormone is a pituraty product that has no single easily identifiable target endocrine gland
but it is the most important hormone for postnatal growth. attainment of size depends on it
what does growth hormone do (4)
a) promotes bone lengthening by stimulating matutatio and mitosis of chondrocytes
b) promotes protein sysnthesis in tissues, esp muslces and organs. this facilatates tissue englargemnt
c) stims glucneogeneis by increasing hepatic glucose and inhibiting glucose uptake (anti-insulin). thus is diabetogenic
d) stims lipolysis (increases fat metabolism)
how does GH exert its effects?
by chemical messengers that are released and induced by GH: IGF-1 and IGF-2.
IGF-1 is more important. Plasma concentrations of IGF-1 reflect
IGF-2 is more invalid in fetbal devlopmetn, but insulin also plays an important role
GH acts on the liver and other tissues to secrete IGF-1 into blood and locally
children who's e growth is more rapid than average have higher than average concentrations of IGF-1
in GH receptor defect, the treatment is synthetic IGF-1
the IGF-1 receptor...
has tyrosisn kinase activity, similar to the insulin.
recent evidneces suggest that IGF-1 acts locals in an autocirine or paracrine manner to stim cell divisions and bone growth and that IGF-1 in the circulation plays only a minor role, if any, in stimulating growth.
what is the main sources of IGF-1 in the blood?
and its function is to regular GH secretion by negative feedback
for IGF-1 and 2 are bound tighty to binding proteins
whats the deal with sleep and GH
in males, there are large rises in plasma GH in the early hours of sleep (max: a large pulse). males secrete most of the their Gh during sleep
in females, there are large pulses throughout the day that don't necessarily correlate to sleep. females secrete more of the GH during the day
stress, excerise, fasting, low plasma glucose, etc can also lead to pulses
GH secretion is active throughout life, but most active in adolescence growth spurts
as quality of sleep deteriorates in the elderly, the amount of GH decreases
GH secretion is stimued by...
by GHRH and inhibited by SS
GHRH provides the primary driver. in its absence, secretion of GH ceases
SS reduces or blocks secretions i reponse to GHRH, but has little influence on synthesis
Gh secetion is controlled by the classic long and short loops neg feed back mechanism
Pulsatility appears to be the result of intermittent secretion of both GHRH and SS
pathway on growth 3 (SEE in mentioned in lecture?0
its the long and short loop thing i probably need to learn
effect of other hormones on growth (4)
insulin and throid hormones and glucocorticods and sex steroids
more to come in nc
describe throids on linear growth
throid hormones: linear growth is stunted in kids with a deficiency of throid hormones. has no effect in absence of GH. deficiency leads to stunted growth. it acts by increases GH synthesis and the number of GHRH-R on soma tropes. makes soma topes more responsive to GHRH
secibre insluin on linear growth
insulin: during fetal growth, it is insulin and not GH or throid hormones that serves as growth-promointg hormones. (insulin doesn't need a binding protein).
IGF-II stims growth of pan creative mass, release of insulin stims growth
insulin is closely relates to IGF 1 and 2 and can active IGF-1-R
sex steroids on linear growth
responsible for dramatic growth spurt at puberty
act by increasing GH and IGF-1
estogen: resposnibe for both acceleration of growth at bingeing of puberty and the closure of the epiphysis at end of puberty
aromatase (converters androgens to E) is required. children (of either sex) lacking do no experience growth spurts)
gonal steroids limits final height by accerlaerting closure fate of epiphysis
descibre gluccoritcos in linear growth
require for synthesis of GH and normal growth
BUT, excressive glucocoritioc decreases GH secetion and antagonizes its effects
adolecnce gwoth is attribuatble to sex steroids from the gonads and perhaps the adrenal
while gonadal steroid promotes linear growth, they also accelerate closure of the epiphysis and therefor limi the final heigh that be obtained.
recent observations who that is is estrogens, rather than androgens that both accelerate growth at puberty and for the epiphyseal plates
children of either sex lacking the aromatase do not experience the pubertal growth
most o f the increase in height stimulated by estorgens or androgens at puberty is due to increased secretion of GH, and thus IGF-1
_____ are required for synthesis of GH and normal growth
gentic factors of height
do mid parental height
then add or subtract 2.5 inches
extreme of Gh secretion (hyper in this nc)
before puberty, it causes gigantismse (since GH promotes bone lengthening)
after puberty, it causes acromegaly, a syndrome characterized by disfiguring bone thickening, enlargement of hands and feet, protrusion of lower jaw, increased body hair and glucose intolerance
deficiency of GH
in children= failure to grown, short stature, mild obesity and delayed puberty
could be from lack of somatotropes, lack of GHRH, failure to generate IGF in liver, or Gh recrotre deficiency
lecture: IGF-1 in plasma... IGF-1 made by tissues...
igf-1 in plasma is made by liver for feedback
ifg-1 made by tissue and bones acts in autocrine/paracine for growth
fyi from lecture
its not just IGF-1, but GH may have a direct role too
fri from lecture
clearly can't measure GH in a single dose because of the episodic burst
eitehr do a 24 hour average, but that blows clinically
so often it is induced by e.g. argine, and see if you get desired results
what stims the hypothalamus for GH?
argine, exerise, stress, fasting, low plama gluscose, sleep