Just take the little white levothyroxine pill every day and you'll be fine. With just one TSH test a year. Yes, sure, when you get papers actually identifying that Growth Hormone and Thyroid Stimulating Hormone at the finest timescales. Like this:
These non-genomic actions of T3 on GH and TSH synthesis/secretion may have an important physiological relevance for the optimal control of the rate of GH and TSH basal secretion, minute by minute.
I have long thought the only way we could ever even approach proper thyroid dosing is with an implanted device capable of releasing extremely tiny amounts of thyroid hormone - T4 and T3. It has always struck me that the most difficult single problem is the control mechanism: - How does it "know" the dosing required? How can it analyse its environment accurately?
Review
Novel aspects of T3 actions on GH and TSH synthesis and secretion: physiological implications
Paula Bargi-Souza, Francemilson Goulart-Silva and Maria Tereza Nunes⇑
P Bargi-Souza, Physiology and Biophysics, University of São Paulo, Institute of Biomedical Sciences, São Paulo, Brazil
F Goulart-Silva, Physiology and Biophysics, University of São Paulo, Institute of Biomedical Sciences, São Paulo, Brazil
M Nunes, Physiology and Biophysics, University of São Paulo, Institute of Biomedical Sciences, São Paulo, Brazil
Abstract
Thyroid hormones (TH) classically regulate gene expression by transcriptional mechanisms. In pituitary, the encoding genes for Growth Hormone (GH) and Thyroid Stimulating Hormone (TSH) are examples of genes regulated by triiodothyronine (T3) in a positive and negative way, respectively. Recent studies have shown a rapid adjustment of GH and TSH synthesis/secretion induced by T3 posttranscriptional actions. In somatotrophs, T3 promotes an increase in Gh mRNA content, poly(A) tail length and binding to the ribosome, associated with a rearrangement of actin cytoskeleton. In thyrotrophs, T3 reduces Tshb mRNA content, poly(A) tail length and its association to the ribosome. In parallel, it promotes a redistribution of TSH secretory granules to more distal regions of the cell periphery, indicating a rapid effect of T3 inhibition of TSH secretion. T3 was shown to affect the content of tubulin and the polymerization of actin and tubulin cytoskeletons in the whole anterior pituitary gland, and to increase intracellular alpha (CGA) content. This review summarizes genomic and non-genomic/posttranscriptional actions of TH on the regulation of several steps of GH and TSH synthesis and secretion. These distinct mechanisms induced by T3 can occur simultaneously, even though non-genomic effects are promptly elicited and precede the genomic actions, coexisting in a functional network within the cells.
Received 29 March 2017
Revision received 4 September 2017
Accepted 26 September 2017
Accepted Preprint first posted online on 26 September 2017
Full paper (at least in draft form) available here: