In clinical practice, frequently supplementation with synthetic or natural thryroid hormone is used. This inevitably results in a low TSH because of feedback inhibition by triiodothyronine (T3) on synthesis and release of T4 from the thyroid gland. Endocrinologists often express a concern that "the TSH is too low", ie below the accepted clinical range. None have been able to explain to me what are the long term consequences of having a low TSH in and of itself. What is too low? Since it must be expected in thyroid supplementation, I fail to see the concern, and I cannot find relevant publications that would explain to me the ramification of low TSH. I call on the world-wide expertise of ResearchGate participants.
According to current textbook knowledge the main site of TSH production is the thyrotrope cell of the anterior lobe of the pituitary. However, numerous studies with mammalian and avian species have shown that another part of the pituitary, the so-called pars tuberalis (PT) also synthesizes and secretes TSH . The deduced amino acid sequence for the alpha and beta subunit seems to be identical in the pars tuberalis cells and the thyrotropes. However, the regulation is very different, while and PT- derived TSH is under control of melatonin receptors and does not react to TRF, the thyrotropes respond to TRF but not to melatonin. The target of the PT-derived TSH is a circumscript region in the wall of the third ventricle and TSH receptors regulate the activitity of DIO2 and DIO3. For a review,see Yasuo S, Korf HW Gen Comp Endocrinol. 172: 15-22 (2011)
I appreciate the response. i will look up your reference. What do you mean by DIO2 and 3? many thanks
Wilfrid Raby
These are the enzymes deiodinase type 2 (DIO2) converting T4 to T3 and deiodinase type 3 (DIO 3) converting T3 to T2. You should also look up our paper in PNAS (Ono H et al.: Proc. Natl. Acad Sci 105: 18238-18242
The uptake of T3 and T4 into different tissues varies. T4 is readily taken up by the brain cells, whereas T3 is more easily absorbed by the liver, kidneys and heart. Therefore the required level of TSH, regulating one's own production of hormones, depends on the medication used. If it is Thyroxin (T4) by itself, then TSH should be kept at a level where own production is still possible to allow higher levels of T3 and T2. If medication is animal dessicated thyroid, then typically TSH is consided best when very low. With some patients, however additional small T4 supplementation is still necessary to keep possible depressive symptoms at bay.
thank you very informative. Is TSH not found within neurons as a neuropeptide, and is its synthesis depend on t4 levels?
To the best of my knowledge, TSH is only synthesized in thyrothrope cells of hypophysial pars distalis (PD, adenohypophysis) and the hypopyhsial pars tuberalis. It is not synthesized in neurons. What you probably mean TRF which indeed is synthesized and secreted from peptidergic neurons and controls TSH secretion from the PD but not from the PT.
Though not synthesized by the neuron, thyroid hormones are known to play critical role in potentiating the process of myelination, therefore the state state of TSH will be of importance in neurodegenerating disorders
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