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| Verfasst von: | Feger, Martina [VerfasserIn]  |
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| | Meier, Leonie [VerfasserIn] |
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| | Strotmann, Jörg [VerfasserIn] |
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| | Hoene, Miriam [VerfasserIn] |
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| | Vogt, Julia [VerfasserIn] |
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| | Wisser, Alexandra [VerfasserIn] |
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| | Hirschle, Susanna [VerfasserIn] |
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| | Kheim, Marie-Jo [VerfasserIn] |
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| | Hocher, Berthold [VerfasserIn] |
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| | Weigert, Cora [VerfasserIn] |
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| | Föller, Michael [VerfasserIn] |
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| Titel: | Endothelin receptor B-deficient mice are protected from high-fat diet-induced metabolic syndrome |
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| Verf.angabe: | Martina Feger, Leonie Meier, Jörg Strotmann, Miriam Hoene, Julia Vogt, Alexandra Wisser, Susanna Hirschle, Marie-Jo Kheim, Berthold Hocher, Cora Weigert, Michael Föller |
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| E-Jahr: | 2024 |
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| Jahr: | February 2024 |
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| Umfang: | 10 S. |
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| Fussnoten: | Online verfügbar: 28. Dezember 2023, Artikelversion: 8. Januar 2024 ; Gesehen am 11.03.2025 |
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| Titel Quelle: | Enthalten in: Molecular metabolism |
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| Ort Quelle: | Oxford [u.a.] : Elsevier, 2012 |
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| Jahr Quelle: | 2024 |
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| Band/Heft Quelle: | 80(2024) vom: Feb., Artikel-ID 101868, Seite 1-10 |
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| ISSN Quelle: | 2212-8778 |
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| Abstract: | Objective - Endothelin receptor B (ETB) together with ETA mediates cellular effects of endothelin 1 (ET-1), an autocrine and endocrine peptide produced by the endothelium and other cells. It regulates vascular tone and controls kidney function. Metabolic syndrome is due to high caloric intake and is characterized by insulin resistance, dyslipidemia, and white adipose tissue (WAT) accumulation. ETA/ETB antagonism has been demonstrated to favorably influence insulin resistance. Our study explored the role of ETB in metabolic syndrome. - Methods - Wild type (etb+/+) and rescued ETB-deficient (etb−/−) mice were fed a high-fat diet, and energy, glucose, and insulin metabolism were analyzed, and hormones and lipids measured in serum and tissues. Cell culture experiments were performed in HepG2 cells. - Results - Compared to etb+/+ mice, etb−/− mice exhibited better glucose tolerance and insulin sensitivity, less WAT accumulation, lower serum triglycerides, and higher energy expenditure. Protection from metabolic syndrome was paralleled by higher hepatic production of fibroblast growth factor 21 (FGF21) and higher serum levels of free thyroxine (fT4), stimulators of energy expenditure. - Conclusions - ETB deficiency confers protection from metabolic syndrome by counteracting glucose intolerance, dyslipidemia, and WAT accumulation due to enhanced energy expenditure, effects at least in part dependent on enhanced production of thyroid hormone/FGF21. ETB antagonism may therefore be a novel therapeutic approach in metabolic syndrome. |
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| DOI: | doi:10.1016/j.molmet.2023.101868 |
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| URL: | Bitte beachten Sie: Dies ist ein Bibliographieeintrag. Ein Volltextzugriff für Mitglieder der Universität besteht hier nur, falls für die entsprechende Zeitschrift/den entsprechenden Sammelband ein Abonnement besteht oder es sich um einen OpenAccess-Titel handelt.
kostenfrei: Volltext: https://doi.org/10.1016/j.molmet.2023.101868 |
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| | kostenfrei: Volltext: https://www.sciencedirect.com/science/article/pii/S2212877823002028 |
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| | DOI: https://doi.org/10.1016/j.molmet.2023.101868 |
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| Datenträger: | Online-Ressource |
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| Sprache: | eng |
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| Sach-SW: | FGF21 |
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| | Insulin |
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| | Thyroid hormone |
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| | Triglyceride |
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| K10plus-PPN: | 1919504583 |
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| Verknüpfungen: | → Zeitschrift |
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Endothelin receptor B-deficient mice are protected from high-fat diet-induced metabolic syndrome / Feger, Martina [VerfasserIn]; February 2024 (Online-Ressource)
