Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Experiment Videos

Sequential deiodination of thyroxine in human thyroid gland.

H Ishii, M Inada, K Tanaka

    The Journal of Clinical Endocrinology and Metabolism
    |November 1, 1982
    PubMed
    Summary

    Thyroid tissues from Graves' disease patients show accelerated conversion of thyroxine (T4) to 3,3'-diiodothyronine (3,3'-T2). This study demonstrates enhanced iodothyronine deiodination in Graves' thyroids, impacting thyroid hormone metabolism.

    Related Concept Videos

    You might also read

    Related Articles

    Articles linked to this work by shared authors, journal, and citation graph.

    Sort by
    Same author

    Increased expression levels of tensin3 mRNA in thyroid functional adenomas as compared to non-functioning adenomas.

    Experimental and clinical endocrinology & diabetes : official journal, German Society of Endocrinology [and] German Diabetes Association·2008
    Same author

    Expression of S100A2 and S100A6 in thyroid carcinomas.

    Histopathology·2005
    Same author

    Lower concentration of serum soluble CD8 in severe Hashimoto's disease.

    Clinical and experimental immunology·2004
    Same author

    Decrease of CD154 intensity on peripheral CD4+ T cells in autoimmune thyroid disease.

    Clinical and experimental immunology·2004
    Same author

    Tie-1 tyrosine kinase expression in human thyroid neoplasms.

    Histopathology·2004
    Same author

    PGP9.5 mRNA could contribute to the molecular-based diagnosis of medullary thyroid carcinoma.

    European journal of cancer (Oxford, England : 1990)·2004

    Area of Science:

    • Endocrinology
    • Biochemistry
    • Thyroidology

    Background:

    • Thyroid hormones, thyroxine (T4) and triiodothyronine (T3), are crucial regulators of metabolism.
    • Iodothyronine deiodinases are key enzymes that activate or inactivate thyroid hormones.
    • Alterations in deiodinase activity are implicated in thyroid disorders like Graves' disease.

    Purpose of the Study:

    • To investigate and characterize iodothyronine deiodinase activities in human thyroid tissues.
    • To compare deiodination pathways in normal thyroid glands versus those from patients with Graves' disease.
    • To elucidate the specific roles of 5-deiodinase and 5'-deiodinase in thyroid hormone metabolism in Graves' disease.

    Main Methods:

    • Incubation of human thyroid tissues (normal and Graves' disease) with iodothyronines (T4, T3, rT3).

    Related Experiment Videos

  • Measurement of deiodination products (rT3, T3, 3,3 2) using radioimmunoassays (RIAs).
  • Kinetic analysis (Km, Vmax) and determination of optimal reaction conditions (pH, temperature, cofactors, inhibitors).
  • Main Results:

    • Both inner ring (5-deiodination) and outer ring (5'-deiodination) monodeiodination activities were identified in human thyroids.
    • Deiodination reactions were dependent on time, tissue volume, temperature, pH, and dithiothreitol concentration.
    • Graves' disease thyroid tissues exhibited significantly higher conversion rates of T4 to rT3 and overall T4 to 3,3 2 compared to normal thyroids.
    • Specific kinetic parameters (Km, Vmax) were determined for T3 and rT3 conversion to 3,3 2.

    Conclusions:

    • Human thyroid glands possess both 5-deiodinase and 5'-deiodinase activities.
    • Graves' disease is associated with accelerated iodothyronine deiodination, particularly the conversion of T4 to 3,3 2 via T3 or rT3.
    • These findings highlight altered thyroid hormone metabolism in Graves' disease, potentially contributing to the hyperthyroid state.