Please use this identifier to cite or link to this item: https://scidar.kg.ac.rs/handle/123456789/8243
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dc.rights.licenseBY-NC-ND-
dc.contributor.authorPetrović, Ivica-
dc.contributor.authorPejnović, Nada-
dc.contributor.authorLjujic, Biljana-
dc.contributor.authorPavlovic S.-
dc.contributor.authorMiletic Kovacevic, Marina-
dc.contributor.authorJeftic, Ilija-
dc.contributor.authordjukic, aleksandar-
dc.contributor.authorDraginic N.-
dc.contributor.authorAndjic M.-
dc.contributor.authorArsenijevic, Nebojsa-
dc.contributor.authorLukic, Miodrag-
dc.contributor.authorJovicic, Nemanja-
dc.date.accessioned2020-09-19T15:10:48Z-
dc.date.available2020-09-19T15:10:48Z-
dc.date.issued2020-
dc.identifier.urihttps://scidar.kg.ac.rs/handle/123456789/8243-
dc.description.abstract© Copyright © 2020 Petrovic, Pejnovic, Ljujic, Pavlovic, Miletic Kovacevic, Jeftic, Djukic, Draginic, Andjic, Arsenijevic, Lukic and Jovicic. Aims/Hypothesis: Galectin 3 appears to play a proinflammatory role in several inflammatory and autoimmune diseases. Also, there is evidence that galectin 3 plays a role in both type-1 and type-2 diabetes. During obesity, hematopoietic cell-derived galectin 3 induces insulin resistance. While the role of galectin 3 expressed in islet-invading immune cells in both type-1 and type-2 diabetes has been studied, the importance of the expression of this molecule on the target pancreatic β cells has not been defined. Methods: To clarify the role of galectin 3 expression in β cells during obesity-induced diabetogenesis, we developed transgenic mice selectively overexpressing galectin 3 in β cells and tested their susceptibility to obesity-induced type-2 diabetes. Obesity was induced with a 16-week high-fat diet regime. Pancreatic β cells were tested for susceptibility to apoptosis induced by non-esterified fatty acids and cytokines as well as parameters of oxidative stress. Results: Our results demonstrated that overexpression of galectin 3 increases β-cell apoptosis in HFD conditions and increases the percentage of proinflammatory F4/80+ macrophages in islets that express galectin 3 and TLR4. In isolated islets, we have shown that galectin 3 overexpression increases cytokine and palmitate-triggered β-cell apoptosis and also increases NO2−-induced oxidative stress of β cells. Also, in pancreatic lymph nodes, macrophages were shifted toward a proinflammatory TNF-α-producing phenotype. Conclusions/Interpretation: By complementary in vivo and in vitro approaches, we have shown that galectin 3-overexpression facilitates β-cell damage, enhances cytokine and palmitate-triggered β-cell apoptosis, and increases NO2−-induced oxidative stress in β cells. Further, the results suggest that increased expression of galectin 3 in the pancreatic β cells affects the metabolism of glucose and glycoregulation in mice on a high-fat diet, affecting both fasting glycemic values and glycemia after glucose loading.-
dc.rightsopenAccess-
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/4.0/-
dc.sourceFrontiers in Endocrinology-
dc.titleOverexpression of Galectin 3 in Pancreatic β Cells Amplifies β-Cell Apoptosis and Islet Inflammation in Type-2 Diabetes in Mice-
dc.typearticle-
dc.identifier.doi10.3389/fendo.2020.00030-
dc.identifier.scopus2-s2.0-85079628459-
Appears in Collections:Faculty of Medical Sciences, Kragujevac

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