Sick euthyroid syndrome is associated with decreased TR expression and DNA binding in mouse liver
Abstract
Infection is associated with low serum thyroid hormones and thyrotropin levels. Here we demonstrate that infection also reduces thyroid hormone receptor (TR) expression. In gel shift experiments, retinoid X receptor (RXR)/TR DNA binding was reduced in mouse liver by 60 and 77%, respectively, 4 and 16 h after lipopolysaccharide (LPS) administration. Surprisingly, LPS did not decrease either TR-α or TR-β protein levels at 4 h, but by 16 h TR-α 1, TR-α 2, and TR-β levels were reduced by 55, 87, and 41%, respectively. We previously reported that LPS rapidly decreases RXR protein levels in liver. Therefore, we added RXR-β to hepatic nuclear extracts prepared 4 h after LPS treatment, which restored RXR/TR DNA binding to a level comparable to that of controls. A similar experiment conducted on extracts prepared 16 h after LPS administration did not restore RXR/TR DNA binding. We propose that decreased RXR expression is limiting for RXR/TR DNA binding at 4 h, whereas the reduction in both TR and RXR levels results in further decreased binding at 16 h.
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Liver TRα and TRβ expression in rodents decrease during acute illness but not during chronic inflammation and bacterial sepsis.
“Liver TRα and TRβ expression in rodents decrease during acute illness [15, 39] but not during chronic inflammation and bacterial sepsis.”
From An update on non-thyroidal illness syndrome (2021) · cites this paper as [39]
Liver TRβ1 expression decreases during acute inflammation in mice and limited availability of SRC-1 might be partly responsible for the illness induced decrease of liver DIO1.
“Indeed, liver TRβ1 expression decreases during acute inflammation in mice [15, 39, 77] and limited availability of SRC-1, a shared coactivator for TR and inflammatory signaling pathways, might be partly responsible for the illness induced decrease of liver DIO1 [78, 79].”
From An update on non-thyroidal illness syndrome (2021) · cites this paper as [39]
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References 45 · Cited by 64
- Authors
- Beigneux, A. P., Moser, A. H., Shigenaga, J. K., Grunfeld, C., & Feingold, K. R.
- Affiliations
- San Francisco VA Medical Center (US)
- Department of Medicine, University of California San Francisco and Metabolism Section, Medical Service, Department of Veterans Affairs Medical Center, San Francisco, California 94121
- ORCID
- Beigneux, Anne P.
- Venue
- American Journal of Physiology-Endocrinology and Metabolism
- Publisher
- American Physiological Society
- Published
- 2003-01-01
- Volume
- 284
- Issue
- 1
- Pages
- E228-E236
- ISSN
- 0193-1849 (ISSN-L)
- 1522-1555
- OpenAlex
- W2168047609
- Cited by
- 64
- References
- 45
- Citations by year
- 2026: 1 · 2025: 1 · 2023: 2 · 2022: 1 · 2020: 2 · 2019: 3 · 2018: 2 · 2017: 1 · 2016: 4 · 2015: 3 · 2014: 1 · 2013: 2 · 2012: 2
- FWCI
- 2.24
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- American Journal of Physiology-Endocrinology and Metabolism (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (5r01dk049448-04, 5r01ar039639-09)
- National Institute of Diabetes and Digestive and Kidney Diseases (DK-49448)
- National Institute of Arthritis and Musculoskeletal and Skin Diseases (AR-39639)
- Topics
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Thyroid Disorders and Treatments
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Estrogen and related hormone effects
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adrenal Hormones and Disorders
- Keywords
- low T3 syndrome, thyroid hormone receptor, retinoid X receptor, lipopolysaccharide, infection, liver, hepatic gene expression
- MeSH terms
- Animals, DNA, Escherichia coli, Euthyroid Sick Syndromes, Female, Kinetics, Lipopolysaccharides, Liver, Malate Dehydrogenase, Mice, Inbred C57BL, Nuclear Proteins, Proteins, Receptors, Thyroid Hormone, RNA, Messenger, Transcription Factors, Gene Expression, Receptors, Retinoic Acid, Dimerization, Protein Isoforms, Response Elements, Thyroid Hormone Receptors alpha, Thyroid Hormone Receptors beta, Retinoid X Receptors, Mice
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