TNFα is a key trigger of inflammation in diet-induced non-obese MASLD in mice.

Autor:	Burger K; Department of Nutritional Sciences, Molecular Nutritional Science, University of Vienna, Vienna, Austria., Jung F; Department of Nutritional Sciences, Molecular Nutritional Science, University of Vienna, Vienna, Austria., Baumann A; Department of Nutritional Sciences, Molecular Nutritional Science, University of Vienna, Vienna, Austria., Brandt A; Department of Nutritional Sciences, Molecular Nutritional Science, University of Vienna, Vienna, Austria., Staltner R; Department of Nutritional Sciences, Molecular Nutritional Science, University of Vienna, Vienna, Austria., Sánchez V; Department of Nutritional Sciences, Molecular Nutritional Science, University of Vienna, Vienna, Austria., Bergheim I; Department of Nutritional Sciences, Molecular Nutritional Science, University of Vienna, Vienna, Austria. Electronic address: ina.bergheim@univie.ac.at.
Jazyk:	angličtina
Zdroj:	Redox biology [Redox Biol] 2023 Oct; Vol. 66, pp. 102870. Date of Electronic Publication: 2023 Sep 01.
DOI:	10.1016/j.redox.2023.102870
Abstrakt:	Tumor necrosis factor alpha (TNFα) is thought to be a critical factor in the development of metabolic dysfunction-associated steatotic liver disease (MASLD). Here, we determined the effects of a treatment with the anti-TNFα antibody infliximab and a genetic deletion of TNFα, respectively, in the development of non-obese diet-induced early metabolic dysfunction-associated steatohepatitis (MASH) in mice. The treatment with infliximab improved markers of liver damage in mice with pre-existing early MASH. In TNFα -/- mice, the development of early signs of MASH and insulin resistance was significantly attenuated compared to wild-type animals. While mRNA expression of proinflammatory cytokines like interleukin 1β (Il1b) and interleukin 6 (Il6) were significantly lower in livers of MASH-diet-fed TNFα -/- mice compared to wild-type mice with early MASH, markers of intestinal barrier function were similarly impaired in both MASH-diet-fed groups compared to controls. Our data suggest that TNFα is a key regulator of hepatic inflammation and insulin resistance associated with the development of early non-obese MASH. Competing Interests: Declaration of competing interest All authors declare no conflict of interest. (Copyright © 2023 The Authors. Published by Elsevier B.V. All rights reserved.)
Databáze:	MEDLINE
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