Hormones I

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Darwin's experiment Cap on tip - no bending Conclusion - tip sense light, response elsewhere New Hypothesis: Chem. substance transported
Steroids Cholesterol Test/Oest/Cortisol
Peptides GH, PTH, Oxytocin
Amino Acids TH, catecholeamines
Endocrine -FDBCK External stimulus Hypothalamus Releasing hormone AP Tropic hormone Hormone
Pituitary gland function Releases hormones that regulate other hormone glands
Tumour Only grow upward, sits in skeletal fossa, compresses optic nerve
Where is A.P? Always same size as optic chiasma
P.P. hormones Oxytocin/ADH
P hormone release Produced in paraventricular + supraoptic nucleus Travel intraxonally Stored in axon terminals Released into CB when + by action potential from pituitary
Oxytocin MOA Binds to R Raises IC [Ca2+] Acts as 2' mess. Triggers myoepithelial cells of mammary glands to contract
Neuroendocrine reflex of milk secretion Suckling-> Hypo -> p.p. -> oxytocin -> milk ejection
A.P. hormones FLAT PG FSH gonads gonadotrophs LH gonads gonadotrophs ATCH adrenal glands corticotrophs TSH Thyroid gland Thyrotrophs Prolactin Mammary glands Lactotrophs GH Bone/skel. muscle somatotrophs
Hypothalamus control of A.P. GCTG SD GnRH -> FSH/LH Corticotropin RH -> ACTH TRH -> TSH GHRH -> GH SS -| Prolactin DA -| Anterior pituitary
Posterior lobe circulation Neurohypophysis Neurosecretory cell transport hormone to P.P.
Anterior lobe circulation Portal vein connects pituitary + hypothalamic CB
Direct met. effects of GH Anabolic Opposes insulin, stims cells to converse glucose for CNS.
Effects on muscle Decreased glucose uptake Increase aa uptake/pro synth. Increased muscle mass
Effects on adipose tissue Decreased glucose uptake increased lipolysis Decrease in fat deposits
Effects on liver Increased gluconeogenesis Increased protein synthesis Stimulates IGF production
Indirect growth promoting effect of GH GH-> Liver -> IGF -> skeletal growth/bone deposition/cartilage formation -> Soft tissue growth / protein synthesis/ cell proliferation
When does bone response cease? When growth plates fuse
Somatopause Decrease in LBM Decrease in bone mineral density Increase in body fat
- FDBCK of this External conditions Hypothalamus Releasing Hormone AP GH Liver IGF-1,2
Gigantism Excessive IGF while epiphyseal growth plates are open
Acromegaly Excessive GH after fusion of epiphysis Cardiomegaly Diabetes due to anti-insulin action
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