Please use this identifier to cite or link to this item:
https://scidar.kg.ac.rs/handle/123456789/9199
Full metadata record
DC Field | Value | Language |
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dc.rights.license | openAccess | - |
dc.contributor.author | Pejnović, Nada | - |
dc.date.accessioned | 2020-09-19T17:43:12Z | - |
dc.date.available | 2020-09-19T17:43:12Z | - |
dc.date.issued | 2015 | - |
dc.identifier.issn | 1820-8665 | - |
dc.identifier.uri | https://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.rights | info:eu-repo/semantics/openAccess | - |
dc.rights.uri | https://creativecommons.org/licenses/by-nc-nd/4.0/ | - |
dc.source | Serbian Journal of Experimental and Clinical Research | - |
dc.title | Galectin-3 in obesity and type 2 diabetes | - |
dc.type | article | - |
dc.identifier.doi | 10.1515/SJECR-2015-0057 | - |
dc.identifier.scopus | 2-s2.0-84950244419 | - |
Appears in Collections: | Faculty of Medical Sciences, Kragujevac |
Files in This Item:
File | Description | Size | Format | |
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10.1515-SJECR-2015-0057.pdf | 2.46 MB | Adobe PDF | View/Open |
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