The role of glucocorticoids in the regulation of thyroid function in man
Open accessAbstract
The diurnal variation in thyroidal iodine release previously observed in euthyroid subjects appears to correlate with variations in serum immunoassayable thyrotropin (TSH). The hypothesis is advanced that this diurnal rhythm seems to be primarily regulated by a negative feedback action of circulating hydrocortisone. The administration of maintenance doses of hydrocortisone to patients with primary adrenal insufficiency and pharmacological doses to euthyroid subjects was accompanied by an acute suppression in both thyroidal iodine release and serum TSH values. An escape from glucocorticoid suppression was observed to occur in 2 or 3 days with the resumption of a near-normal thyroidal iodine release rate but was accompanied by a dampening or absence of the normal diurnal rhythm. Withdrawal of pharmacological doses of glucocorticoids in euthyroid subjects and maintenance doses in primary hypoadrenal patients was accompanied by transient stimulation of both serum TSH and thyroidal iodine release values. The study of a patient before and after cryohypophysectomy indicated that the rebound response in thyroid release after steroid withdrawal may be a useful testing procedure to indirectly assess the hypothalamicpituitary reserve capacity of TSH.
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High glucocorticoid levels suppress the pituitary response to TRH in man, and glucocorticoid treatment is associated with downregulation of TR neurons in the human PVN.
“Hypothalamic TRH is also modulated by glucocorticoids, as high glucocorticoid levels suppress the pituitary response to TRH in man [69], while a postmortem study in human hypothalamus showed that glucocorticoid treatment is associated with downregulation of TR neurons in the human PVN [14].”
From An update on non-thyroidal illness syndrome (2021) · cites this paper as [69]
The citation to this paper [69] supports the first clause, not the separate postmortem finding cited to [14]. In the Discussion (page unavailable), the paper attributes glucocorticoid suppression to reduced hypothalamic TRF secretion, rather than a suppressed pituitary response to TRF; it also notes that glucocorticoids did not inhibit TRF’s direct action on the rat pituitary. (LLM, conf=0.84)
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- Authors
- Nicoloff, J. T., Fisher, D. A., & Appleman, M. D.
- Affiliations
- University of Southern California (US)
- Venue
- Journal of Clinical Investigation
- Published
- 1970-10-01
- Volume
- 49
- Issue
- 10
- Pages
- 1922-1929
- ISSN
- 0021-9738 (ISSN-L)
- PMC
- PMC322682
- OpenAlex
- W2112972977
- Cited by
- 261
- References
- 14
- Citations by year
- 2026: 1 · 2025: 2 · 2024: 5 · 2023: 10 · 2022: 7 · 2021: 2 · 2020: 6 · 2019: 5 · 2018: 3 · 2017: 1 · 2016: 4 · 2015: 1 · 2014: 7 · 2013: 4 · 2012: 4
- FWCI
- 9.01
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Clinical Investigation (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Thyroid Disorders and Treatments
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adrenal Hormones and Disorders
- Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
- Keywords
- glucocorticoids, cortisol, thyroid function, diurnal cycle, thyroid-stimulating hormone, negative feedback, Addison's disease, glucocorticoid withdrawal, hypothalamic-pituitary-thyroid axis
- MeSH terms
- Adrenal Gland Diseases, Circadian Rhythm, Feedback, Humans, Hydrocortisone, Iodine, Prednisolone, Thyroid Gland, Thyrotropin, Thyroxine-Binding Proteins
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