Overexpression of Galectin 3 in Pancreatic β Cells Amplifies β-Cell Apoptosis and Islet Inflammation in Type-2 Diabetes in Mice

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 e...

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Vydané v:Frontiers in endocrinology (Lausanne) Ročník 11; s. 30
Hlavní autori: Petrovic, Ivica, Pejnovic, Nada, Ljujic, Biljana, Pavlovic, Sladjana, Miletic Kovacevic, Marina, Jeftic, Ilija, Djukic, Aleksandar, Draginic, Nevena, Andjic, Marijana, Arsenijevic, Nebojsa, Lukic, Miodrag L., Jovicic, Nemanja
Médium: Journal Article
Jazyk:English
Vydavateľské údaje: Switzerland Frontiers Media S.A 07.02.2020
Predmet:
Animals
apoptosis
Apoptosis - genetics
Cells, Cultured
Diabetes Mellitus, Experimental - complications
Diabetes Mellitus, Experimental - genetics
Diabetes Mellitus, Experimental - metabolism
Diabetes Mellitus, Type 2 - complications
Diabetes Mellitus, Type 2 - genetics
Diabetes Mellitus, Type 2 - metabolism
Endocrinology
galectin 3
Galectin 3 - genetics
inflammation
Inflammation - genetics
Inflammation - metabolism
Inflammation - pathology
Insulin-Secreting Cells - metabolism
Insulin-Secreting Cells - physiology
Islets of Langerhans - metabolism
Islets of Langerhans - pathology
Male
Mice
Mice, Inbred C57BL
Mice, Transgenic
Organ Specificity - genetics
Pancreatitis - genetics
Pancreatitis - metabolism
type-2 diabetes
β cells
apoptosis
inflammation
type-2 diabetes
galectin 3
β cells
ISSN:1664-2392, 1664-2392
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Shrnutí: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. 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. 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 NO -induced oxidative stress of β cells. Also, in pancreatic lymph nodes, macrophages were shifted toward a proinflammatory TNF-α-producing phenotype. By complementary and approaches, we have shown that galectin 3-overexpression facilitates β-cell damage, enhances cytokine and palmitate-triggered β-cell apoptosis, and increases NO -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.
Bibliografia:ObjectType-Article-1
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Edited by: GianLuca Colussi, University of Udine, Italy
This article was submitted to Translational Endocrinology, a section of the journal Frontiers in Endocrinology
Reviewed by: Abir Mukherjee, Royal Veterinary College (RVC), United Kingdom; Stanislava Stosic-Grujicic, University of Belgrade, Serbia
ISSN:1664-2392
1664-2392
DOI:10.3389/fendo.2020.00030