ECE2022 Poster Presentations Thyroid (136 abstracts)
Deiodinase Type I regulation in fatty liver disease
Nuria López Alcántara 1 , Cathleen Geißler 2 , Alison-Michelle Naujack 2 , Yingfu Chen 3 , Natalie Taege 2 , Jan H. Britsemmer 2 , Leonardo Vinicius Monteiro De Assis 4 , Henrik Oster 4 , Joachim Spranger 3 , Eva Wirth 3 , Rubén Nogueiras 5 , Henriette Kirchner 2 & Jens Mittag 1
1University of Lubeck, Center of Brain, Behavior and Metabolism (CBBM), Institute of Endocrinology, Lübeck, Germany; 2 University of Lubeck, Center of Brain, Behavior and Metabolism (CBBM), Institute of Human genetics. Section Epigenetics and Metabolism, Lübeck, Germany; 3Charité - Universitätsmedizin Berlin, Center for Cardiovascular Research, Berlin, Germany; 4University of Lubeck, Center of Brain, Behavior and Metabolism (CBBM), Institute of Neurobiology, Lübeck, Germany; 5University of Santiago de Compostela, Molecular Metabolism, Santiago de Compostela, Spain
Background and Aim: Hepatic thyroid hormone (TH) signalling plays an important role in onset and progression of liver diseases. Patients with altered thyroid hormone regulation in the liver, leading to a local hypothyroid, are at higher risk of developing non-alcoholic fatty liver disease (NAFLD). Treatment with thyroid hormones proved to be a promising therapy for these patients, slowing the progression of NAFLD to non-alcoholic steatohepatitis (NASH), a more advanced stage of the disease characterized by inflammation and occasional fibrosis. The action of thyroid hormone in the liver is regulated by TH transporters, deiodinases, and receptors. Among these, deiodinase type 1 (Dio1) is a major player, converting the prohormone thyroxine (T4) directly to the bioactive form T3 in the hepatocytes. However, the exact regulation of Dio1 in liver disease is not yet fully understood.
Methods: We studied Dio1 expression in several hepatic disease models, including male C57BL/6 mice fed with high-fat diet (HFD) during 18 weeks and treated with metformin for the last two weeks of treatment, male C57BL/6 mice fed with methionine-choline-deficient HFD for 2 weeks, male C57BL/6 mice fed with choline-deficient HFD for 4 and 8 weeks at thermoneutrality, and finally male C57BL/6 mice treated with carbon tetrachloride to induce liver failure.
Results: Expression of Dio1 was rapidly increased in animals fed with HFD and remained elevated throughout the treatment without changes induced by metformin treatment. Remarkably, some of the other conditions did not resulted in an increase in Dio1, although lipid deposition in the liver was similar.
Conclusion: Our results show that Dio1 is rapidly induced by HFD, an effect that seems to be independent of insulin sensitivity, as it was not reversed by metformin treatment. However, Dio1 induction was restrained in other animal models with similar degree of hepatic lipid deposition, suggesting that other factors such as liver inflammation may prevent the HFD induced Dio1 induction.
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Endocrine Abstracts
ISSN 1470-3947 (print) | ISSN 1479-6848 (online)
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