If you want someone to appreciate the detailed interactions for thyroid hormones and gene expression, perhaps get reincarnated as a frog!
Obviously, this paper is directly relevant only to frogs and related species. However, what it does, is to discuss the thyroid hormones and receptors in terms of true signalling. Whereas in the context of humans, almost all the discussion treats thyroid hormone more like a nutrient. That is, in terms of cells requiring thyroid hormone in much the same way as they do oxygen and energy supplies.
Further, it points out that one tissue will respond in one fashion, and another in a very different fashion.
Certainly this is all to do with development rather than our adult state. But I do feel that there might well be lessons to be learned from shifting viewpoint.
Front Endocrinol (Lausanne). 2019; 10: 143.
Published online 2019 Mar 14. doi: 10.3389/fendo.2019.00143
PMCID: PMC6426756
Tail Resorption During Metamorphosis in Xenopus Tadpoles
Yoshio Yaoita*
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Abstract
Tail resorption in anuran tadpoles is one of the most physically and physiologically notable phenomena in developmental biology. A tail that is over twice as long as the tadpole trunk is absorbed within several days, while concurrently the tadpole's locomotive function is continuously managed during the transition of the driving force from the tail to hindlimbs. Elaborate regulation is necessary to accomplish this locomotive switch. Tadpole's hindlimbs must develop from the limb-bud size to the mature size and the nervous system must be arranged to control movement before the tail is degenerated. The order of the development and growth of hindlimbs and the regression of the tail are regulated by the increasing levels of thyroid hormones (THs), the intracellular metabolism of THs, the expression levels of TH receptors, the expression of several effector genes, and other factors that can modulate TH signaling. The tail degeneration that is induced by the TH surge occurs through two mechanisms, direct TH-responsive cell death (suicide) and cell death caused by the degradation of the extracellular matrix and a loss of cellular anchorage (murder). These pathways lead to the collapse of the notochord, the contraction of surviving slow muscles, and, ultimately, the loss of the tail. In this review, I focus on the differential TH sensitivity of the tail and hindlimbs and the mechanism of tail resorption during Xenopus metamorphosis.
Thanks for posting this interesting paper. It illustrates the vital role of t3 and I agree that is strikes a chord amongst those of us who would like to see this more widely recognised and not just in the tadpole fraternity.
This is very interesting! More so because I have 5 xenopus in a large tank in my front room, they are amazing frogs, from the first pregnancy tests to ongoing vital research. Amazing.
Haha glad you enjoyed it, I'm full of the unexpected :). Just a disclaimer I do not conduct research on my xenopus, they are pets, in case anyone worries lol.
Well, it just so happens that in my Blue Horizon Thyroid genetic DNA results, the issue of signalling came up with regard to the Thyrotropin Releasing Hormone Receptor (TRHR). The result was double G (guanine neucleotide) in the red (for potential 'danger') zone, indicating that it is either the wild type, with no genetic variations, or inherited from both parents.
This was the explanation:
'The 'G' result has been associated with a less responsive negative feedback mechanism. Carriers of this genotype may show higher circulating TSH:T3/4 ratio due to delayed reduction of TRH and TSH in the presence of healthy thyroid hormone levels. This may mean that the body is subjected to a less efficient response to changing thyroid hormone requirements.'
I asked for a further explanation, given that I have low in-range FT3 and FT4 and mid-range TSH (I'll be having this retested today) and this was the response:
'The ‘G’ result of the TRHR gene could certainly point towards central hypothyroidism due to poor signalling between the hypothalamus and pituitary. The hypothalamus produces TRH which in turn stimulates the production of TSH by the pituitary. The ‘G’ result in TRHR can confer lower receptivity to TRH which could then reduce production of TSH. A simple but helpful intervention would be to increase blood flow to the brain.'
Whilst the poor signalling is higher up the 'chain' it seemingly has an impact on the thyroid hormones further down the chain. I wonder how this would translate in the example of the frog!? Maybe end up with half a tail?
Not sure what was meant in the above explanation by 'A simple but helpful intervention would be to increase blood flow to the brain' - it makes it sound so straightforward but they didn't say what the treatment should be and certainly didn't suggest taking T4 or T3..... Maybe I should start standing on my head?
It is the DNA Blue Thyroid Genetic Panel. I would be cautious using it for dio2 as the interpretation may not be detailed enough. I found that there were some inconsistencies in information and contradictions but also some confirmations and surprises. If it would help, I could PM my results to you to give you an idea of how the info is presented. BH are very happy for people to query results and ask for clarifications free of charge.
I was actually going to ask for details of which gene/SNP you are referring to? Purely out of interest - not saying I would know anythng at all about it.
It provides the specific genes associated with thyroid functions (in this case TRHR), the result and advice/explanation (not very detailed and standard phrasing). Happy to send you the report for context and further info. Curiously, I also have problems with the FKBP5 gene, to do with cortisol regulation and lowered stress resilience, which also has an impact on thyroid hormone levels.
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