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Cited by 161Thyroid Disorders and TreatmentsProtein Interaction Studies and Fluorescence AnalysisGrowth Hormone and Insulin-like Growth Factors

Increased thyroxine turnover and thyroidal function after stimulation of hepatocellular binding of thyroxine by phenobarbital

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Oppenheimer, Jack H., Bernstein, Gerald, Surks, Martin I.·1968·Journal of Clinical Investigation
DOI 10.1172/jci105831PMC PMC297295
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Abstract

Administration of phenobarbital to rats in a dosage schedule previously demonstrated to increase hepatocellular binding of thyroxine results in increased hormonal turnover, due both to increased deiodination and to fecal disposition of thyroxine iodine. The rate of biliary excretion of thyroxine iodine is roughly proportional to the hepatic content of exchangeable thyroxine. The enhanced peripheral disposition of thyroxine appears to lead to increased thyroidal function, as measured by isotopic iodine studies, and the maintenance of a normal nonradioactive serum PBI. On the other hand, thyroidectomized animals maintained on a constant replacement dose of L-thyroxine and treated with phenobarbital exhibit a marked fall in serum PBI. These findings suggest that increased thyroxine flux in phenobarbital-treated animals is secondary to primary stimulation of hepatocellular binding. Exchangeable intracellular thyroxine may thus be an important determinant of hormone turnover and, possibly, of hormonal action.

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  • The effect of phenobarbital to increase T4 and T3 metabolism has been documented in rodents and humans, but effects on thyroid function are more notable in rats.

    “The effect of phenobarbital to increase T 4 and T3 metabolism has been documented in rodents (173) and humans (174,175), but effects on thyroid function are more notable in rats (172).”

    From Guidelines for the Treatment of Hypothyroidism: Prepared by the American Thyroid Association Task Force on Thyroid Hormone Replacement (2014) · cites this paper as [173]

    The Results (Thyroid function, Table III; page unavailable) report increased thyroidal activity in phenobarbital-treated rats, supporting the rat-specific effect cited as (172). The paper does not compare that effect with thyroid function in humans, so it does not establish that the effect is more notable in rats. The human-metabolism portion is attributed to separate citations (174, 175). (LLM, conf=0.84)

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Authors
Oppenheimer, J. H., Bernstein, G., & Surks, M. I.
Affiliations
Albert Einstein College of Medicine (US)
Venue
Journal of Clinical Investigation
Publisher
American Society for Clinical Investigation
Published
1968-06-01
Volume
47
Issue
6
Pages
1399-1406
ISSN
0021-9738 (ISSN-L)
DOI
10.1172/jci105831
PMC
PMC297295
OpenAlex
W2054942726
Cited by
161
References
22
Citations by year
2024: 1 · 2023: 1 · 2022: 2 · 2021: 1 · 2016: 1 · 2015: 1 · 2014: 2 · 2013: 3 · 2012: 3
FWCI
9.14
Type
journal article
Language
en
Open access
Locations
  • Journal of Clinical Investigation (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Thyroid Disorders and Treatments
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Interaction Studies and Fluorescence Analysis
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Growth Hormone and Insulin-like Growth Factors
Keywords
phenobarbital, thyroxine, deiodination, biliary excretion, iodine, thyroid function, thyroidectomy, thyroxine replacement
MeSH terms
Animals, Bile, Blood Proteins, Chlordan, Iodine, Iodine Radioisotopes, Kidney, Liver, Male, Phenobarbital, Protein Binding, Thyroid Gland, Thyroidectomy, Thyroxine, Rats

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