I wouldn't expect to see this available anytime soon since the understanding of just exactly what T2 does is still very limited but it is interesting to note they are working on developing testing. PR
Background: 3,5-Diiodo-L-thyronine (3,5-T2), a potential metabolite of 3,3′,5-triiodothyronine (T3), exerts marked metabolic actions without the undesirable cardiac and central side effects of T3. So far the lack of reliable quantification methods for endogenous 3,5-T2 in human serum has limited further insight into its physiological and pathophysiological roles in endocrine homeostasis and disease status.
Conclusion: The established CLIA is highly specific, sensitive, precise and accurate for 3,5-T2 detection in human serum. Because 3,5-T2 is not regulated in conditions of an altered thyroid state, it is most likely that serum 3,5-T2 concentrations are not directly dependent on feedback regulation via the hypothalamic–pituitary axis. In addition 3,5-T2 is present in thyroidectomized individuals on T4 substitution, and it is elevated after T4 substitution compared with healthy controls. We conclude that these data support extrathyroidal production of 3,5-T2 from T4.
The current knowledge about T2 is that it doesn't bind much to the T4/3 receptors in the cells, so isn't a factor in controlling T3 production, but it has a direct effect on the mitochondria, which are the energy-producing complexes in he cells. How it controls this energy production is a bit unclear at the moment, but it certainly stands apart from the usual pituitary-thyroid-body cell relationship of T4 and T3. Whether it is important in controlling energy output is made problematic because people on T4 have more T2 - but people on T4 don't always respond well to monotherapy - so the study in future should be to see if people who don't respond well to T4 therapy don't get elevated T2 unless they are given T3 as well, whereas those who do, have elevated T2. This way, we could find another piece in the jigsaw.
Diogenes, that brings up another question. You said "T4/3" receptors. Dr. Tata in his article a couple of years ago said they thought there were some T4 receptors but that there wasn't a clear picture of the situation. Most of what I have read always refers to T3 receptors. Do we have a clear picture of where, or when, T3 binds as opposed to where, or when, T4 binds? PR
There is eg an old paper that describes something about T3 and T4 binding to receptors:
Proc. Nat. Acad. Sci. USA
Vol. 70, No. 12, pp. 3488-3492, December 1973
Thyroid Hormone Action in Cell Culture: Demonstration of
Nuclear Receptors in Intact Cells and Isolated Nuclei
(receptor/thyroxine/triiodothyronine)
HERBERT H. SAMUELS AND JIR S. TSAI
T3 is always by far the most important, but T4 may have minor specialized roles to play. The problem always is: you can show in cell culture that T4 binds to some receptors, but does it do so in the wole intact organism? Wrenching the back off the clock doesn't necessarily help you in finding out how it works.
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Direct and rapid effects of 3,5-diiodo-L-thyronine (T2)
Confused T3/T2
