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Thyroid hormone metabolism and nuclear binding in Gunn rats
T Komaki1, S Sakata, K Kamikubo
1Department of Internal Medicine, Hashima Municipal Hospital, Japan.
Journal of Endocrinological Investigation
|May 1, 1991
Summary
In Gunn rats, lower conversion of thyroxine (T4) to triiodothyronine (T3) leads to reduced T3 levels and increased T4 and reverse T3. Nuclear T3 binding and TSH secretion remain unaffected.
Area of Science:
- Endocrinology
- Molecular Biology
- Animal Models
Background:
- Thyroid hormone metabolism is crucial for physiological regulation.
- Gunn rats (j/j) exhibit a genetic defect affecting thyroid hormone processing.
- Understanding thyroid hormone conversion is key to metabolic research.
Purpose of the Study:
- To investigate thyroid hormone profiles in homozygous Gunn rats (j/j) compared to heterozygous controls (j/+).
- To assess the activity of hepatic T4 5'-deiodinase, the enzyme responsible for T3 production.
- To evaluate the binding of T3 to hepatic nuclei in both rat models.
Main Methods:
- Measurement of serum total and free thyroid hormones (T3, T4, rT3) and TSH.
- Assay of hepatic T4 5'-deiodinase activity in microsomal fractions.
- Determination of T3 binding to hepatic nuclei using binding constants and maximal binding capacities.
Main Results:
- Homozygous Gunn rats (j/j) showed significantly lower serum total and free T3 levels.
- Serum total T4 and free T4 levels were elevated in j/j rats after 15 days of age.
- Hepatic T4 5'-deiodinase activity was significantly reduced in j/j rats, indicating impaired T4 to T3 conversion.
Conclusions:
- Decreased conversion of T4 to T3 is a primary factor for altered thyroid hormone levels in j/j rats.
- Elevated serum T4 and reverse T3, along with low T3, are consequences of impaired deiodination.
- Nuclear T3 binding and pituitary TSH secretion appear to be normal in homozygous Gunn rats.