control of growth Flashcards
what cells produce growth hormone
somatotroph cells
what tissue does growth hormone target
all tissues
what % of the pituitary gland comprises of somatorophs
40-50%
growth hormone synthesis pathway (from hypothal)
neurons in arcuate nucleus of hypothal secrete GHRH -> hyophyseal portal blood -> GHRH binds to G-protein couples receptors on somatotrophs -> activates Gα -> adenyl cyclase activation -> increase cAMP leading to gene transcription and synthesis of GH
how is GH released from cells
PKA allows Ca2+ Chs to open -> C2+ enters cell -> vesicles containing GH are exocytosed
what hormone can inhibit GH secretion and where is it produced
somatostatin can inhibit GH secretion, it is produced in the periventricular region of the hypothal
what is the role of IGF-1 in the GH cycle
negative feedback -> GH produced IGF-1 which in turn inhibits GH at the hypothal. and pit. levels
how does ghrelin affect GH
increases hypothalamic GHRH production which thus increases GH production
role of oestrogen in GH axis
- inhibit the release of IGF-1 fro the liver (GH release is not inhibited)
- potentiate pituitary GH response to pulses of GHRH
- mute inhibition from somatostatin
- potentiates ghrelin’s action
how do somatotroph cells change throughout ife
the characteristics and number remain the same but their secretion pattern changes
what are the characteristics of GH secretion
- rhythmic characteristics -> secretion occurs in a pulsatile manor every 2hrs
- circaidian rhythm affects GH secretion -> maximum release at night
when do maximum GH levels occur in the course of a day
at night -> within minutes of slow wave sleep
what physiological factors also affect GH secretion
gender; age; pubertal status
3 physiological causes for GH secretion
- in response to hyogycaemia being sensed by the hypothalamus
- in response to exercide, stress, trauma etc.
- secretion during puberty
4 direct effects of GH
- stimulation of cellular metabolism leading to tissue growth
- releases fatty acids from adipose tissue
- promotes gluconeogeneis + glycogenolysis
- insulin resistance -> decreases glucose uptake and ultilisation by target tissues -> increase [blood glucose] ->diabetogenic