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SGLT-2 inhibitors and GLP-1 receptor agonists in metabolic dysfunction-associated fatty liver disease

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dc.contributor.authorMoon, Jun Sung-
dc.contributor.authorHong, Jun Hwa-
dc.contributor.authorJung, Yong Jin-
dc.contributor.authorFerrannini, Ele-
dc.contributor.authorNauck, Michael A.-
dc.contributor.authorLim, Soo-
dc.date.accessioned2022-09-29T03:18:29Z-
dc.date.available2022-09-29T03:18:29Z-
dc.date.created2022-06-16-
dc.date.issued2022-06-
dc.identifier.citationTrends in Endocrinology and Metabolism, Vol.33 No.6, pp.424-442-
dc.identifier.issn1043-2760-
dc.identifier.urihttps://hdl.handle.net/10371/184649-
dc.description.abstract© 2022 Elsevier LtdMetabolic dysfunction-associated fatty liver disease (MAFLD) is a chronic condition that affects nearly one billion people globally, characterized by triacylglycerol accumulation in the liver as a consequence of metabolic abnormalities (obesity and impaired glucose regulation). Low-grade inflammation, oxidative stress, mitochondrial dysfunction, and dysbiosis in gut microbiota are involved in the etiology of MAFLD, and both cardiovascular events and hepatic complications are the long-term consequences. In the absence of approved therapies for this condition, sodium–glucose cotransporter 2 inhibitors (SGLT-2 Is) and glucagon-like peptide 1 receptor agonists (GLP-1 RAs) have the specific advantage of lowering body weight and providing cardiovascular benefits. Here, we discuss potential roles for SGLT-2 Is and GLP-1 RAs in the prevention and treatment of intrahepatic triacylglycerol accumulation and associated inflammation and/or fibrosis.-
dc.language영어-
dc.publisherElsevier BV-
dc.titleSGLT-2 inhibitors and GLP-1 receptor agonists in metabolic dysfunction-associated fatty liver disease-
dc.typeArticle-
dc.identifier.doi10.1016/j.tem.2022.03.005-
dc.citation.journaltitleTrends in Endocrinology and Metabolism-
dc.identifier.wosid000800447500006-
dc.identifier.scopusid2-s2.0-85129636553-
dc.citation.endpage442-
dc.citation.number6-
dc.citation.startpage424-
dc.citation.volume33-
dc.description.isOpenAccessN-
dc.contributor.affiliatedAuthorLim, Soo-
dc.type.docTypeReview-
dc.description.journalClass1-
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