ArticleFrontiers in physiology2017
Both 3,5-Diiodo-L-Thyronine and 3,5,3'-Triiodo-L-Thyronine Prevent Short-term Hepatic Lipid Accumulation via Distinct Mechanisms in Rats Being Fed a High-Fat Diet.
Article in Frontiers in physiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 26 citations in OpenAlex.
- Prolactin and Triiodothyronine Modulate Seasonal Variation in Brown Adipose Tissue in Djungarian Hamsters.Journal of experimental zoology. Part A, Ecological and integrative physiology · 2026Article
- Co-Morbid Hypothyroidism and Liver Dysfunction: A Review.Clinical medicine insights. Endocrinology and diabetes · 2024Review
- Lipid Metabolism in Pregnancy Women with Hypothyroidism and Potential Influence on Pregnancy Outcome.Journal of lipids · 2024Review
- Influence of Altered Thyroid Hormone Mechanisms in the Progression of Metabolic Dysfunction Associated with Fatty Liver Disease (MAFLD): A Systematic Review.Metabolites · 2022Review
- Novel insights into the pathological development of dyslipidemia in patients with hypothyroidism.Bosnian journal of basic medical sciences · 2022Review
- Effects of Thyroid Hormones on Lipid Metabolism Pathologies in Non-Alcoholic Fatty Liver Disease.Biomedicines · 2022Review
- Update on dyslipidemia in hypothyroidism: the mechanism of dyslipidemia in hypothyroidism.Endocrine connections · 2022Review
- [New development for targeted therapy of non-alcoholic fatty liver disease with thyroid hormone receptor beta].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2021Article
- 3,5-Diiodo-L-Thyronine (T2) Administration Affects Visceral Adipose Tissue Inflammatory State in Rats Receiving Long-Lasting High-Fat Diet.Frontiers in endocrinology · 2021Article
- Hypothyroidism and Nonalcoholic Fatty Liver Disease: Pathophysiological Associations and Therapeutic Implications.Journal of clinical and translational hepatology · 2020Review
- Hypothyroidism-Induced Nonalcoholic Fatty Liver Disease (HIN): Mechanisms and Emerging Therapeutic Options.International journal of molecular sciences · 2020Review
- Genomic and Non-Genomic Mechanisms of Action of Thyroid Hormones and Their Catabolite 3,5-Diiodo-L-Thyronine in Mammals.International journal of molecular sciences · 2020Review
- The role of thyroid hormone in metabolism and metabolic syndrome.Therapeutic advances in endocrinology and metabolism · 2020Review
- miR-22-3p is involved in gluconeogenic pathway modulated by 3,5-diiodo-L-thyronine (T2).Scientific reports · 2019Article
- Thyroid Hormones, Thyromimetics and Their Metabolites in the Treatment of Liver Disease.Frontiers in endocrinology · 2018Review
- A Renewed Focus on the Association Between Thyroid Hormones and Lipid Metabolism.Frontiers in endocrinology · 2018Review
- 3,5-Diiodothyronine: A Novel Thyroid Hormone Metabolite and Potent Modulator of Energy Metabolism.Frontiers in endocrinology · 2018Review
- Similarities and Differences in the Peripheral Actions of Thyroid Hormones and Their Metabolites.Frontiers in endocrinology · 2018Review
- Relationship between Hypothyroidism and Non-Alcoholic Fatty Liver Disease: A Systematic Review and Meta-analysis.Frontiers in endocrinology · 2017Article
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10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
3,3',5-triiodo-L-thyronine (T3) improves hepatic lipid accumulation by increasing lipid catabolism but it also increases lipogenesis, which at first glance appears contradictory. Recent studies have shown that 3,5-diiodothyronine (T2), a natural thyroid hormone derivative, also has the capacity to stimulate hepatic lipid catabolism, however, little is known about its possible effects on lipogenic gene expression. Because genes classically involved in hepatic lipogenesis such as SPOT14, acetyl-CoA-carboxylase (ACC), and fatty acid synthase (FAS) contain thyroid hormone response elements (TREs), we studied their transcriptional regulation, focusing on TRE-mediated effects of T3 compared to T2 in rats receiving high-fat diet (HFD) for 1 week. HFD rats showed a marked lipid accumulation in the liver, which was significantly reduced upon simultaneous administration of either T3 or T2 with the diet. When administered to HFD rats, T2, in contrast with T3, markedly downregulated the expression of the above-mentioned genes. T2 downregulated expression of the transcription factors carbohydrate-response element-binding protein (ChREBP) and sterol regulatory element binding protein-1c (SREBP-1c) involved in activation of transcription of these genes, which explains the suppressed expression of their target genes involved in lipogenesis. T3, however, did not repress expression of the TRE-containing ChREBP gene but repressed SREBP-1c expression. Despite suppression of SREBP-1c expression by T3 (which can be explained by the presence of nTRE in its promoter), the target genes were not suppressed, but normalized to HFD reference levels or even upregulated (ACC), partly due to the presence of TREs on the promoters of these genes and partly to the lack of suppression of ChREBP. Thus, T2 and T3 probably act by different molecular mechanisms to achieve inhibition of hepatic lipid accumulation.
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