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Rat liver and kidney microsomal fractions contain 5'-deiodinase, converting thyroxin into 3,5,3'-triiodothyronine. In control animals a marked decrease in thyroxin concentration takes place when the blood passes through the liver and kidney (triiodothyronine level being preserved). Fasting causes a prominent decrease in blood thyroxin, a small decrease in triiodothyronine as well as a drop of glucose and insulin levels. At the same time a decrease in thyroxin deiodinase activity takes place in the liver; as for the kidney a decrease is less marked. Fasting rats have no gradients in the blood passing through the liver and kidney; triiodothyronine balance remains unchanged. The results show that the rat liver and kidney deiodinase activity regulation (during changes in the body physiological status) helps to maintain triiodothyronine optimum concentration in general circulation.
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Abstract In seasonal rodents, reproduction is activated by a long photoperiod. Furthermore, maintaining an inhibitory short photoperiod for over 20 weeks triggers a spontaneous reactivation of the gonadotropic axis called photorefractoriness. Photoactivation is proposed to involve melatonin, hypothalamic thyroid hormones (TH) and (Arg) (Phe)-amide peptides. The mechanisms involved in photorefractoriness are so far unknown. We analyzed the dynamic changes in long photoperiod- and photorefractory-induced activation of reproduction in both Syrian and Djungarian hamsters to validate the current model of photoactivation and to uncover the mechanisms involved in photorefractoriness. We detected a conserved early inhibition of expression of the TH catabolizing enzyme deiodinase 3 (Dio3) in tanycytes, associated with a late decrease of the TH transporter MCT8. This suggests that an early peak of hypothalamic TH may be involved in both photoinduced and photorefractory reactivation. In photoactivation, Dio3 downregulation is followed by an upregulation of Dio2, which is not observed in photorefraction. The upregulation of (Arg) (Phe)-amides occurs several weeks after the initial Dio3 inhibition. In conclusion, we uncovered a so far unreported early inhibition of Dio3. This early downregulation of Dio3 is reinforced by an upregulation of Dio2 in photoactivated hamsters. In photorefractoriness, the Dio3 downregulation might be sufficient to reactivate the gonadotropic axis.
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An antiarrhythmic drug, amiodarone, contains 37% iodine by weight and is structurally similar to the thyroid hormones. The drug inhibits hepatic 5'-deiodinase, resulting in increases in serum thyroxin and "reverse" triiodothyronine, whereas the concentration of triiodothyronine in serum is decreased. There is a significant incidence of either hypothyroidism or hyperthyroidism in patients who are being treated with the drug. This is largely the effect of iodine released from the drug during chronic therapy, but in susceptible individuals amiodarone may unmask autoimmune thyroid disease. Some effects of the drug suggest that it may interfere with the action of thyroid hormones at the cellular level, inducing a state of localized hypothyroidism.
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Decreased quality of life is described more often in hypothyroid patients, who are treated with a synthetic form of thyroxine (L-T4), than in euthyroid controls. A combination of L-T4 and a synthetic form of triiodothyronine (L-T3) has been suggested; however, previous meta-analyses on unselected patients did not find any effect. Recent studies demonstrate, that the overall hypothalamic-pituitary-thyroid-tissue homeostasis could be more complex than previously suggested. Polymorphisms in deiodinase and thyroid hormone transporter genes could theoretically explain, why a minor subgroup of hypothyroid patients seem to have an effect of L-T4/L-T3 combination therapy.
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The rapid increase in serum thyroxine (T4), triiodothyronine (T3) and reverse triiodothyronine (rT3) in the pig shortly birth presumably due to enhanced secretory activity of the thyroid gland was observed. During the 2nd and 3rd week of live T3 and T4 remained essentially unchanged but rT3 continued to rise to a high plateau level. This resulted in an increase in rT3/T4 ratio to about two and rT3/T3 raio to about one. A shift to rT3 production seems to be a reflection of an increased capacity of 5-iodothyronine deiodinase with age.
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