Chronic treatment with palmitic acid increases superoxide content and apoptosis of BRIN-BD11 cells with participation of NADPH oxidase, without GPR40 involvement.

Author(s)

Eloísa Aparecida Vilas Bôas

• Document type: Master's Dissertation
• Press: São Paulo.
• Institution: Universidade de São Paulo (USP). Instituto de Ciências Biomédicas (ICB/SDI)
• Defense date: 2013-10-16

Examining board members

Angelo Rafael Carpinelli; Anna Karenina Azevedo Martins; Fernanda Ortis

• Advisor: Angelo Rafael Carpinelli

Abstract

Chronic exposure to saturated fatty acids can lead to pancreatic beta cell dysfunction, reduction of insulin secretion and apoptosis, condition known as lipotoxicity, that has been related to: endoplasmic reticulum stress, chronic stimulation of GPR40 and increased production of reactive oxygen species (ROS) from, among other sources, the enzime NADPH oxidase. We intended to explore as mechanisms of lipotoxicity: reticulum stress, chronic stimulation of GPR40 and NADPH oxidase generation of ROS, as well as relations between NADPH oxidase and reticulum stress. Our results show that chronically palmitic acid induced an increase in the superoxide, in part from NADPH oxidase. NADPH oxidase inhibition by VAS2870 reverted the apoptosis induced by chronic exposure to palmitic acid, and was related to a lower expression of a reticulum stress marker (PERK). GW9508, GPR40 agonist, did not produced the same effects observed after chronic treatment with palmitic acid, suggesting that activation of GPR40 pathway is not involved in these processes. (AU)

• FAPESP's process: 11/04511-4 - Acute and chronic effects of oleic and palmitic acids and the agonist GW9508 on insulin secretion and oxidative stress of the lineage BRIND-BD11
• Grantee: Eloisa Aparecida Vilas Boas
• Support Opportunities: Scholarships in Brazil - Master