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Redox modulation, function and survival of pancreatic β-cells: evidence on the role of NADPH oxidase-2 (NOX2) enzyme in a model of glucotoxicity in vitro.

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Author(s):
Arnaldo Henrique de Souza
Total Authors: 1
Document type: Doctoral Thesis
Press: São Paulo.
Institution: Universidade de São Paulo (USP). Instituto de Ciências Biomédicas
Defense date:
Examining board members:
Angelo Rafael Carpinelli; Everardo Magalhães Carneiro; Maria Lucia Cardillo Correa Giannella; Lucia Rossetti Lopes; Fernanda Ortis
Advisor: Angelo Rafael Carpinelli
Abstract

Oxidative stress and NADPH oxidase-2 (NOX2) enzyme are associated to the decline of the functional β-cell mass in type 2 diabetes (T2D). Here, we tested the role of NOX2 on β-cell glucotoxicity. NOX2 knockout (NOX2 KO) and wild type (WT) C57BL/6J mice islets were isolated and cultured up to 3 weeks at 10 or 30 mmol/l glucose concentrations (G10 and G30, respectively). The insulin secretion was higher in NOX2-KO vs. WT islets despite similar metabolic and cytosolic glutathione-redox potential (EGSH) changes. The prolonged culture at G30 increases the H2O2 concentration and cytosolic thiol oxidation, followed by increased βcell apoptosis but preserving maximal secretory response. These responses were almost identical in both types of islets. In conclusion, NOX2 is a negative regulator of insulin secretion in C57BL/6J mouse islets, but is not a critical component for β-cell survival in a model of glucotoxicity in vitro. (AU)

FAPESP's process: 11/21299-9 - EFFECTS OF HYPERGLYCEMIA AND HYPERLIPIDEMIA ON INSULIN SECRETION AND NAD(P)H OXIDASE ACTIVITY IN PANCREATIC ISLETS
Grantee:Arnaldo Henrique de Souza
Support type: Scholarships in Brazil - Doctorate