Physiology 3120 Lecture Notes - Lecture 3: Calcitriol, Bone, Biomineralization

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Hardy Lec 3
Hypothalamo-pituitary-thyroid axis (regulate metabolism)
-hypothalamus releases TRH and SRIF  TRH stimulates anterior pituitary to release TSH  TSH
goes to thyroid follicles through bloodstream to stimulate T3/T4 release
-thyroid hormones act over long periods of time to regulate metabolism and HR (more next
lecture)
TRH = thyrotropin releasing hormone
TSH = thyroid stimulating hormone
-if too much T3/T4, negative feedback regulation where receptors on hypothalamus and
anterior pituitary binds to T3/T4 to inhibit further TRH/TSH release
-on top of that, also have SRIF released by hypothalamus into anterior pituitary to inhibit
further TSH release (less common mechanism)
SRIF = somatostatin release inhibiting peptide
NOTE: somatostatin = somatotropin same thing
-TPO has two functions: iodinates and couples
TPO = thyroid peroxidase
1. TPO adds one iodine to tyrosine to give monoiodotyrosine or two iodines to tyrosine to give
diiodotyrosine  randomly occurs
2. TPO then couples either a monoiodotyrosine with diiodotyrosine to give T3 or couples two
diiodotyrosines to give T4
-need to bring in iodine from basolateral side  apical side where TPO is
-Na-I symporter uses Na gradient to drive Na and I transport from blood on basolateral side to
colloid on apical side
-pendrin is symporter on apical side that transports I from parafollicular cell to colloid where
TPO couples TG to I to get Tg-T3/T4
-Tg-T3/T4 complex goes back into cell via pinocytosis
-in parafollicular cell, intracellular enzymes separate T3/T4 from Tg
-T3/T4 leaves via basolateral side to enter bloodstream and bind to thyroid target tissues
TSH Stimulation
-so TSH binds to its receptor on basolateral side to:
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1. Stimulate Na/I symporter activity to bring in more iodine into cell
2. Stimulates thyroglobulin production
3. Stimulates TPO activity to get more Tg iodination
-even though T3/T4 are not steroid hormones, they are not very soluble due to aromatic ring
thus more lipid-loving
-need binding proteins (carrier proteins) to take them to target tissues
-regulate bioavailability because without them, hormones would be able to get to target tissues
-also provide mobility to hormones as they go from tissue to tissue
-thyroid gland secretes more T4 BUT in plasma, there is more T3
-this is because T3 less stable but more potent ie: active  live fast die young
-T4 more stable but less potent ie: active
RMR talked about changing message of hormones en route
-similarly, T4 converted to T3 in cell when needed using deiodinases
-T3/T4 lipid-loving so can easily go through PM
-D2 converts T4 into T3 that enters nucleus to bind to TR (T3-receptor)
-T3-TR complex acts like transcription factor that turns on/off T3-responsive gene
-D2 can also convert T4 into rT3 which is inactive reverse T3
-D3 can also convert T3 into T2 which is a weaker thyroid hormone
 Do not need to worry about above two points just appreciate that T4 can also be converted
into two other weaker thyroid hormones
-TR bound to co-repressors thus no transcription factor thus no transcription of thyroid genes
-T3 binds to TR to displace corepressors to act as transcription factor to allow transcription of
thyroid genes
-T3 recruits coactivators to completely activate transcription of thyroid genes
-cretinism = impaired mental capacity
-increase O2 demand as in more oxygen available when needed
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