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Rapid regulation of thyroid sodium-iodide symporter activity by thyrotrophin and iodine.

Abstract

Transport of iodide into thyrocytes, a fundamental step in thyroid hormone biosynthesis, depends on the presence of the sodium-iodide symporter (NIS). The importance of the NIS for diagnosis and treatment of diseases has raised several questions about its physiological control. The goal of this study was to evaluate the influence of thyroid iodine content on NIS regulation by thyrotrophin (TSH) in vivo. We showed that 15-min thyroid radioiodine uptake can be a reliable measurement of NIS activity in vivo. The effect of TSH on the NIS was evaluated in rats treated with 1-methyl-2-mercaptoimidazole (MMI; hypothyroid with high serum TSH concentrations) for 21 days, and after 1 (R1d), 2 (R2d), or 5 (R5d) days of withdrawal of MMI. NIS activity was significantly greater in both MMI and R1d rats. In R2d and R5d groups, thyroid iodide uptake returned to normal values, despite continuing high serum TSH, possibly as a result of the re-establishment of iodine organification after withdrawal of MMI. Excess iodine (0.05% NaI for 6 days) promoted a significant reduction in thyroid radioiodide uptake, an effect that was blocked by concomitant administration of MMI, confirming previous findings that iodine organification is essential for the iodide transport blockade seen during iodine overload. Therefore, our data show that modulation of the thyroid NIS by TSH depends primarily on thyroid iodine content and, further, that the regulation of NIS activity is rapid.

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  • Authors

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    Source

    The Journal of endocrinology 184:1 2005 Jan pg 69-76

    MeSH

    Animals
    Hypothyroidism
    Iodine
    Male
    Methimazole
    Rats
    Rats, Wistar
    Symporters
    Thyroid Gland
    Thyrotropin
    Time Factors

    Pub Type(s)

    Journal Article
    Research Support, Non-U.S. Gov't

    Language

    eng

    PubMed ID

    15642784

    Citation

    TY - JOUR T1 - Rapid regulation of thyroid sodium-iodide symporter activity by thyrotrophin and iodine. AU - Ferreira,Andrea C F, AU - Lima,Lívia P, AU - Araújo,Renata L, AU - Müller,Glaucia, AU - Rocha,Renata P, AU - Rosenthal,Doris, AU - Carvalho,Denise P, PY - 2005/1/12/pubmed PY - 2005/2/26/medline PY - 2005/1/12/entrez SP - 69 EP - 76 JF - The Journal of endocrinology JO - J. Endocrinol. VL - 184 IS - 1 N2 - Transport of iodide into thyrocytes, a fundamental step in thyroid hormone biosynthesis, depends on the presence of the sodium-iodide symporter (NIS). The importance of the NIS for diagnosis and treatment of diseases has raised several questions about its physiological control. The goal of this study was to evaluate the influence of thyroid iodine content on NIS regulation by thyrotrophin (TSH) in vivo. We showed that 15-min thyroid radioiodine uptake can be a reliable measurement of NIS activity in vivo. The effect of TSH on the NIS was evaluated in rats treated with 1-methyl-2-mercaptoimidazole (MMI; hypothyroid with high serum TSH concentrations) for 21 days, and after 1 (R1d), 2 (R2d), or 5 (R5d) days of withdrawal of MMI. NIS activity was significantly greater in both MMI and R1d rats. In R2d and R5d groups, thyroid iodide uptake returned to normal values, despite continuing high serum TSH, possibly as a result of the re-establishment of iodine organification after withdrawal of MMI. Excess iodine (0.05% NaI for 6 days) promoted a significant reduction in thyroid radioiodide uptake, an effect that was blocked by concomitant administration of MMI, confirming previous findings that iodine organification is essential for the iodide transport blockade seen during iodine overload. Therefore, our data show that modulation of the thyroid NIS by TSH depends primarily on thyroid iodine content and, further, that the regulation of NIS activity is rapid. SN - 0022-0795 UR - https://www.unboundmedicine.com/medline/citation/15642784/full_citation L2 - http://joe.endocrinology-journals.org/cgi/pmidlookup?view=long&pmid=15642784 ER -