Regional physiological adaptation of the central nervous system deiodinases to iodine deficiency
Abstract
The goal of the present investigation was to analyze the types 2 (D2) and 3 (D3) iodothyronine deiodinases in various structures within the central nervous system (CNS) in response to iodine deficiency. After 5-6 wk of low-iodine diet (LID) or LID + 2 microg potassium iodide/ml (LID + KI; control), rats' brains were processed for in situ hybridization histochemistry for D2 and D3 mRNA or dissected, frozen in liquid nitrogen, and processed for D2 and D3 activities. LID did not affect weight gain or serum triiodothyronine, but plasma thyroxine (T4) was undetectable. In the LID + KI animals, D3 activities were highest in the cerebral cortex (CO) and hippocampus (HI), followed by the olfactory bulb and was lowest in cerebellum (CE). Iodine deficiency decreased D3 mRNA expression in all CNS regions, and these changes were accompanied by three- to eightfold decreases in D3 activity. In control animals, D2 activity in the medial basal hypothalamus (MBH) was similar to that in pituitary gland. Of the CNS D2-expressing regions analyzed, the two most responsive to iodine deficiency were the CO and HI, in which an approximately 20-fold increase in D2 activity occurred. Other regions, i.e., CE, lateral hypothalamus, MBH, and pituitary gland, showed smaller increases. The distribution of and changes in D2 mRNA were similar to those of D2 activity. Our results indicate that decreases in the expression of D3 and increases in D2 are an integral peripheral component of the physiological respo…
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A reduction in plasma T3 could in theory be compensated for by a homeostatic acceleration of the D2 pathway, increasing locally produced T3.
“A reduction in plasma T3 could in theory be compensated for by a homeostatic acceleration of the D2 pathway, increasing locally produced T3 (44).”
From Treatment Preferences in Patients With Hypothyroidism (2025) · cites this paper as [44]
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- Authors
- Peeters, R., Fekete, C., Goncalves, C., Legradi, G., Tu, H. M., Harney, J. W., Bianco, A. C., Lechan, R. M., & Larsen, P. R.
- Affiliations
- Brigham and Women's Hospital (US)
- Tufts University (US)
- Division of Endocrinology, Diabetes, Metabolism and Molecular Medicine, Department of Medicine, New England Medical Center-Tufts University School of Medicine, Boston, Massachusetts 02111
- Venue
- American Journal of Physiology-Endocrinology and Metabolism
- Publisher
- American Physiological Society
- Published
- 2001-07-01
- Volume
- 281
- Issue
- 1
- Pages
- E54-E61
- ISSN
- 0193-1849 (ISSN-L)
- 1522-1555
- OpenAlex
- W2206735333
- Cited by
- 79
- References
- 6
- Citations by year
- 2025: 3 · 2024: 3 · 2023: 2 · 2022: 2 · 2021: 4 · 2020: 3 · 2019: 5 · 2018: 3 · 2017: 2 · 2016: 3 · 2015: 3 · 2014: 4 · 2013: 2 · 2012: 5
- FWCI
- 2.07
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- American Journal of Physiology-Endocrinology and Metabolism (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institute of Diabetes and Digestive and Kidney Diseases (R01DK044128, R01 DK 44128)
- Topics
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Thyroid Disorders and Treatments
- Physical Sciences › Environmental Science › Health, Toxicology and Mutagenesis › Chemical Analysis and Environmental Impact
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Growth Hormone and Insulin-like Growth Factors
- Keywords
- iodine deficiency, central nervous system, low iodine diet, cerebral cortex, hippocampus, cerebellum, olfactory bulb, medial basal hypothalamus, pituitary gland, thyroid hormone metabolism
- MeSH terms
- Adaptation, Physiological, Animals, Central Nervous System, Diet, Iodide Peroxidase, Iodine, Isoenzymes, Male, Organ Size, RNA, Messenger, Thyroid Gland, Thyroid Hormones, Rats, Sprague-Dawley, In Situ Hybridization, Rats
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