Please use this identifier to cite or link to this item: https://scidar.kg.ac.rs/handle/123456789/9199
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dc.rights.licenseopenAccess-
dc.contributor.authorPejnović, Nada-
dc.date.accessioned2020-09-19T17:43:12Z-
dc.date.available2020-09-19T17:43:12Z-
dc.date.issued2015-
dc.identifier.issn1820-8665-
dc.identifier.urihttps://scidar.kg.ac.rs/handle/123456789/9199-
dc.description.abstract© 2015, University of Kragujevac, Faculty of Science. All rights reserved. Galectin-3 is an important regulator of inflammation and acts as a receptor for advanced-glycation (AGE) and lipoxidation end-products (ALE). Evidence indicates a significant upregulation in circulating levels and visceral adipose tissue production of Galectin-3 in obesity and type 2 diabetes. Recent studies demonstrate development of obesity and dysregulation of glucose metabolism in Galectin-3 “knockout” (KO) mice, which also develop accelerated and more severe pathology in models of atherosclerosis and metabolically-induced kidney damage. Thus, evidence that Galectin-3 is an important player in metabolic disease is accumulating. This review discusses current evidence on the connection between Galectin-3 and metabolic disease, focusing on mechanisms by which this galectin modulates adiposity, glucose metabolism and obesity-associated inflammatory responses.-
dc.rightsinfo:eu-repo/semantics/openAccess-
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/4.0/-
dc.sourceSerbian Journal of Experimental and Clinical Research-
dc.titleGalectin-3 in obesity and type 2 diabetes-
dc.typearticle-
dc.identifier.doi10.1515/SJECR-2015-0057-
dc.identifier.scopus2-s2.0-84950244419-
Appears in Collections:Faculty of Medical Sciences, Kragujevac

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