Iodine deficiency up-regulates monocarboxylate transporter 8 expression of mouse thyroid gland

Iodine deficiency up-regulates monocarboxylate transporter 8 expression of mouse thyroid gland

Another snippet of information about how the thyroid actually works.

My summary:

Iodine doesn't just hop into the thyroid as it passes in the blood stream - there is a special transporter mechanism that does the job.

If you have low/insufficient iodine, the transporter becomes more active.

If you then have sufficient iodine, the transporter becomes less active.

Chin Med J (Engl). 2014 Dec;127(23):4071-6.

Iodine deficiency up-regulates monocarboxylate transporter 8 expression of mouse thyroid gland.

Hu Z1, Zhuo X2, Shi Y2, Liu X2, Yuan J2, Li L2, Sun Y3.

Author information

Abstract

BACKGROUND:

Iodine deficiency is a major factor affecting thyroid auto-regulation, the quantity of iodine may greatly influence the synthesis of thyroid hormones (THs). It has long been believed that TH enters the cell through passive diffusion. Recent studies have suggested that several transporters could facilitate transportation of TH. The monocarboxylate transporter 8 (MCT8) was identified as a very active and specific TH transporter. The purpose of this study was to investigate whether iodine insufficient affected the expression of MCT8 in the thyroid gland.

METHODS:

Sixty BALB/c mice were randomly divided into two groups: control group was fed with standard feed (iodine concentration of 300 µg/kg); while low-iodine (LI) group received iodine-insufficient feed (iodine concentration of 20-40 µg/kg). After 3 months, 10 mice of each group were sacrificed. The remaining 20 mice of each group were kept till 6 months. From the LI group, we randomly selected 15 mice and injected triiodothyronine (T3, 100 µg/kg body weight per day) intraperitoneally for 24, 48 or 72 hours (5 mice for each time-point). Then, all the mice were sacrificed. Mouse serum thyroxine (T4), T3, and thyroid-stimulating hormone (TSH) levels were determined by chemiluminescence immunoassay (CIA). The protein content or messenger RNA (mRNA) level of thyroid MCT8 was measured by Western blotting analysis or real time RT-PCR respectively. MCT8 subcellular location in thyroid tissues was probed with immunohistochemistry (IHC) assay.

RESULTS:

We found that mouse serum T3 and T4 levels decreased and TSH level increased by the end of the third month. Consistent with these findings, there was significant goiter and hypothyroidism in the LI group. Meanwhile, the MCT8 mRNA increased to 1.36-fold of the level in the control group at the 3(rd) month. At 6(th) month, the serum T4 level in LI mice remained at a lower level, and MCT8 mRNA expression continued rising to nearly 1.60-fold compared with the control group. The protein content was also about 3 times higher than that in the control group. IHC results also revealed MCT8 was of higher expression and localized in the cytoplasm of thyroid follicular cells. After providing exogenous T3 to iodine deficient mice, the serum T3 and T4 gradually increased, whereas MCT8 mRNA and protein both started to decrease and returned to the same level as the control group.

CONCLUSION:

There is a compensatory increase in thyroid MCT8 expression to enhance its capability to transport TH from thyroid to the blood circulation in iodine deficient mice.

PMID:

25430451

[PubMed - in process]

ncbi.nlm.nih.gov/pubmed/254...

Earlier related article:

jci.org/articles/view/42113

MCT8 transported issues are implicated in several disorders/syndromes:

rarediseases.org/rare-disea...

Rod

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  • Thanks, Rod, it is interesting.

  • Is this possibly why in Japan where people allegedly consume rather high amounts of iodine from the diet, the levels of thyroid disorder are not at variance from let's say the UK?

  • It does make you wonder, doesn't it?

    It would be good to see an opinion from someone who perhaps understands rather more than do I! :-)

  • I have not been able to find anything published in any medical journal where it has been shown that iodine levels and breast disease are connected. There's the Brownstein (or whatever his name) protocol which alleges that breast tissue is an 'iodine sponge' and ingesting large amounts of iodine will eliminate conditions like fibrocystic breast disease.

    There is nothing in the medical literature that verifies this.

    There is nothing in the literature that indicates any sort of thyroid condition has any effect, positive or negative, on breast cancer either.

    Possibly, based on this mouse study, ingestion of excessive amounts of iodine just results in more urinary excretion.

    I can well believe that tissues, other than the thyroid benefit from optimal, whatever that is, iodine levels.

  • There always appears to be something missing in the iodine discussions.

    At each deiodination of thyroid hormone, T4 to T3, T3 to T2, etc., an iodine atom is released. What happens to that? Does it not become available to the tissue in which the deiodination occurs? Many descriptions suggest that most such iodine makes its way back to the thyroid for re-organification and use in creating new thyroid hormone - but the usual rather wishy-washy way these things are often glossed over.

    It has often looked to me as if somewhere, way back in evolution, everything to do with thyroid started as a means of keeping iodine away from everything else. But at some point the iodine atoms (or compounds containing them) proved to be useful. Therefore, the whole process of building iodine into the relatively innocuous T4, the binding proteins, the mixture of locations at which deiodination occurs, and so on, are as they are largely in order to protect cells from iodine. With the exception of these odd, individual atoms of iodine.

    Rod

  • Fair enough that breastmilk contains iodine and the glands will secrete it at a higher level than is present in the blood. BUT most of the breast tissue is fat. So when the claim is made that 'breast tissue is an iodine sponge' then which breast tissue?

    Also, inactive mammary gland tissue will not, (? logic here of some sort?) be actively concentrating iodine. For why would it do that if milk is not being produced? It makes no sense whatsoever.

    Have you ever read the paper written (I think) in 1924 by a British physician working in India? He correlated poor hygienic conditions to goitre in areas where iodine levels in the water were relatively low. When hygiene was improved, goitre went away. Maybe pathogens of various types (and here's the gut microbiome connection and disrupted bowel flora from toxins and antibiotics) are more a factor in the development of thyroid disease provided there's SOME iodine available.

    By chance I read an archeology paper about a Methodist cemetery from the early to mid 1800s in Ontario (north shore of Lake Ontario). The skeletons were exhumed in order to move them. One of the things the student wrote is that women were emigrating from England to the area. They were vital and alive when they arrived and gradually became sick and lethargic. This is a goitrogenic area after all. I don't think there's enough iodine in the ground water for anyone but women especially seemed to suffer most. As usual. :(

    Actually, cattle could not be raised in this general area until veterinary medicine established their requirement for iodine and selenium (and other things). This is both a selenium and iodine poor region. Beef was imported from the United States. I looked that up too because I was wondering what animals were people raising for meat. Somehow deer manage to live and breed here. Maybe it's a matter of hygiene for them too. They are not restricted to living on dirty farms. Maybe giving cattle supplements somehow compensates for crowded conditions?

  • If you're looking to understand how iodine works in the body, there's a comprehensive chapter in the Tired Thyroid book: amazon.co.uk/gp/product/149... It debunks a lot of the Brownstein/Abraham dogma.

    It addresses Japanese iodine consumption, breast health and iodine, bromine toxicity, etc. Gabkad is correct that iodine should not be found in the breasts of a woman who isn't breastfeeding. BUT, a women who is severely hypothyroid secretes hormones that make her breast similar to that of a breastfeeding woman. Fascinating reading if you're into all that research!

  • I have very low Iodine levels and believe that is why I am not fully well. All other vitamin and mineral levels are good, high in ranges. I have read David Brownstein book and also Lynne Farrow, the Iodine crisis which has a lot of historical info about Iodine being used in the past. Iodine used to be put in bread, they changed it to bromine!! UK stopped that in the 90's but a whole generation has had Bromine instead of Iodine. The bromine blocks Iodine absorption. Milk consumption has gone down-milk is a good source of Iodine. Radiation levels have increased in the last half century. People near Chernobyl were given Iodoral tablets so that their bodies would not absorb radio active iodine. Sheep, here up north, have only recently been free of radiation caused by Chernobyl but the powers that be chose not to tell us that. I could go on!

    It all makes sense to me and I am one week into taking Lugols iodine with some interesting results so far.

    To me the arguments against Iodine don't seem much different to the hysterical arguments against using NDT and folks are split in 2 camps about what is or is not OK.

    I will report back when I feel I have improved or not as the case may be. I am using Genova urine/iodine test to keep an eye on levels.

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