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| Author(s): |
Laila Romagueira Bichara dos Santos
Total Authors: 1
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| Document type: | Doctoral Thesis |
| Press: | São Paulo. |
| Institution: | Universidade de São Paulo (USP). Instituto de Ciências Biomédicas (ICB/SDI) |
| Defense date: | 2010-12-14 |
| Examining board members: |
Angelo Rafael Carpinelli;
Gabriel Forato Anhê;
Everardo Magalhães Carneiro;
Aparecida Emiko Hirata;
Thais Martins de Lima Salgado
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| Advisor: | Angelo Rafael Carpinelli |
| Abstract | |
Fatty acids are required to maintain cellular functioning and are able to modulate insulin secretion from pancreatic islets. The important sites of ROS production are the mitochondria and the NAD(P)H oxidase. The mitochondrial ROS release depends on cellular activity and NAD(P)H oxidase activity depends on many factors, including PKC. Acute (1 hour) exposure to oleic acid increased insulin secretion at 16.7 mM glucose. The insulin secretion induced by OA was associated to increased fatty acid oxidation and decreased glucose metabolism. Also, at 16.7 mM glucose, OA oxidation increased ROS production mediated by NAD(P)H. ROS decreased content induced by NAD(P)H oxidase inhibition induced glucose oxidation re-establishment after OA stimulus. The relative secretion was stimulated by NAD(P)H oxidase inhibition after OA stimulus. This suggests that ROS produced by NAD(P)H oxidase act as glucose metabolism regulators in the pancreatic cell. In consequence of glucose metabolism re-establishment the insulin secretion was increased. In conclusion, ROS produced by NAD(P)H oxidase are regulators of glucose metabolism. The glucose metabolism regulation may be in part responsible for the increased insulin secretion induced by ROS. (AU) | |