Thyroid hormone signaling and the liver
Abstract
Thyroid hormone (TH) plays a critical role in maintaining metabolic homeostasis throughout life. It is well known that the liver and thyroid are intimately linked, with TH playing important roles in de novo lipogenesis, beta-oxidation (fatty acid oxidation), cholesterol metabolism, and carbohydrate metabolism. Indeed, patients with hypothyroidism have abnormal lipid panels with higher levels of low-density lipoprotein levels, triglycerides (triacylglycerol; TAG), and apolipoprotein B levels. Even in euthyroid patients, lower serum-free thyroxine levels are associated with higher total cholesterol levels, LDL, and TAG levels. In addition to abnormal serum lipids, the risk of nonalcoholic fatty liver disease (NAFLD) increases with lower free thyroxine levels. As free thyroxine rises, the risk of NAFLD is reduced. This has led to numerous animal studies and clinical trials investigating TH analogs and TH receptor agonists as potential therapies for NAFLD and hyperlipidemia. Thus, TH plays an important role in maintaining hepatic homeostasis, and this continues to be an important area of study. A review of TH action and TH actions on the liver will be presented here.
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Thyroid hormones can interfere with fibrogenesis by inhibiting TGFb signalling.
“They can also interfere with fi brogenesis by inhibiting TGFb signalling.”
From EASL-EASD-EASO Clinical Practice Guidelines on the management of metabolic dysfunction-associated steatotic liver disease (MASLD). (2024) · cites this paper as [347]
Thyroid hormones reduce hepatic steatosis by stimulating hepatic lipophagy and mitochondrial biogenesis, and by inhibiting hepatic lipogenesis.
“Thyroid hormones reduce hepatic steatosis by stimulating hepatic lipophagy and mitochondrial biogenesis, and by inhibiting hepatic lipogenesis.”
From EASL-EASD-EASO Clinical Practice Guidelines on the management of metabolic dysfunction-associated steatotic liver disease (MASLD). (2024) · cites this paper as [347]
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Tacke, F., Horn, P., Wai-Sun Wong, V., Ratziu, V., Bugianesi, E., Francque, S., Zelber-Sagi, S., Valenti, L., Roden, M., Schick, F., et al. (2024) · Journal of Hepatology · doi:10.1016/j.jhep.2024.04.031 · Cited by 2,210 · see citing works
Nonalcoholic fatty liver disease (NAFLD) from pathogenesis to treatment concepts in humans
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NAFLD and thyroid function: pathophysiological and therapeutic considerations
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Thyroid hormone resistance: mechanisms and therapeutic development
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Exercise Is Medicine for Nonalcoholic Fatty Liver Disease: Exploration of Putative Mechanisms
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- Authors
- Ritter, M. J., Amano, I., & Hollenberg, A. N.
- Affiliations
- Weill Cornell Medicine (US)
- Gunma University (JP)
- Corresponding author
- Hollenberg, Anthony N.
- Venue
- Hepatology
- Published
- 2020-08
- Volume
- 72
- Issue
- 2
- Pages
- 742-752
- ISSN
- 0270-9139 (ISSN-L)
- 1527-3350
- OpenAlex
- W3020477396
- Cited by
- 188
- References
- 122
- Citations by year
- 2026: 21 · 2025: 32 · 2024: 42 · 2023: 38 · 2022: 36 · 2021: 11 · 2020: 8
- FWCI
- 3.57
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- Locations
- Hepatology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institute of Diabetes and Digestive and Kidney Diseases (R01DK117940, DK117940, DK056123)
- Topics
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Thyroid Disorders and Treatments
- Health Sciences › Medicine › Epidemiology › Liver Disease Diagnosis and Treatment
- Health Sciences › Medicine › Surgery › Cholesterol and Lipid Metabolism
- Keywords
- thyroid hormone signaling, liver, hypothyroidism, free thyroxine, non-alcoholic fatty liver disease, hyperlipidemia, lipid metabolism, cholesterol metabolism, fatty acid oxidation, de novo lipogenesis, carbohydrate metabolism, thyroid hormone analogs, thyroid hormone receptor agonists
- MeSH terms
- Animals, Cholesterol, Humans, Liver, Thyroid Hormones, Signal Transduction
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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