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Doctoral Thesis
DOI
10.11606/T.42.2014.tde-19022015-163014
Document
Author
Full name
Maíra Mello Rezende Valle
Institute/School/College
Knowledge Area
Date of Defense
Published
São Paulo, 2014
Supervisor
Committee
Carpinelli, Angelo Rafael (President)
Carvalho, Carla Roberta de Oliveira
Martins, Anna Karenina Azevedo
Nogueira, Fernando Neves
Souza, Kleber Luiz de Araujo e
Title in Portuguese
Alterações na homeostase redox das células beta pancreáticas em resposta à glicose.
Keywords in Portuguese
Espécies reativas de oxigênio
Glicose
Ilhotas pancreáticas
Nox2
Rac1
Sod1
Superóxido
Abstract in Portuguese
As espécies reativas de oxigênio são capazes de influenciar a secreção de insulina, porém ainda não está clara a influência da glicose, principal secretagogo deste hormônio, sobre a homeostase redox das células beta pancreáticas. Incubações por 1 e 48 horas com diferentes concentrações de glicose (2,8; 5,6; 8,3; 11,1; 16,7 e 20 mM) demonstraram que esta é capaz de alterar não só o conteúdo de superóxido, produzido pela mitocôndria e NADPH oxidase, mas também o sistema antioxidante, alterando a concentração de GSH e a expressão das enzimas antioxidantes. Além disso, aumenta a interação Rac1/Sod1, que mantém a NADPH oxidase ativa. Porém, não apresenta endossomas de sinalização redox, os redoxossomas, em resposta a glicose. Estas alterações podem afetar eventos chave para este tecido endócrino, como a secreção de insulina e a morte celular.
Title in English
Modulation of the redox state by glucose in pancreatic beta cells.
Keywords in English
Glucose
Nox2
Pancreatic islets
Rac1
Reactive oxygen species
Sod1
Superoxide
Abstract in English
ROS production in pancreatic beta cells has been associated with the insulin secretion process but the mechanism by which glucose affects the redox state in these cells remains unknown. In order to address this issue, we evaluated the effect of 1 or 48 hours incubation of pancreatic beta cells with various glucose concentrations (2.8, 5.6, 8.3, 11.1, 16.7 and 20 mM). Glucose loading induced superoxide production by mitochondria and NADPH oxidase complex, and enhanced the antioxidant capacity by increasing GSH content and modulate expression of antioxidant enzymes. Glucose also promoted Rac1/Sod1 interaction that maintains NADPH oxidase activated. These cells however did not present redox endosomes, the redoxosomes, in response to glucose loading. These effects might be associated with the process of insulin secretion and pancreatic beta cell death.
 
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Release Date
2017-02-19
Publishing Date
2015-02-20
 
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