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LUCENA, C. F. Fish oil dietary supplementation reduces NAD(P)H oxidase expression and increases SOD1 and SOD2 expression in rat pancreatic islets. 2012. 59 p. Masters thesis (Human Physiology) – Instituto de Ciencias Biomedicas, Universidade de Sao Paulo, Sao Paulo, 2012. Insulin secretion is stimulated by plasma glucose concentration, but circulating fatty acids (FA) may influence the secretory process induced by glucose (GSIS). The oxidation of FA seem to be important for the stimulation of insulin secretion by increasing the production of ATP, although some studies have shown the existence of ATP-dependent and independent pathways for GSIS. The ω-3 polyunsaturated FA affect several physiological processes, such the concentration of plasma lipids, immune and cardiovascular function, peripheral insulin action, neuronal development and visual efficiency. ω-3 FA affect the composition and function of the plasma membrane, signaling and regulation of gene expression in different tissues and promote potent anti-inflammatory action. Considering the important relationship of NAD(P)H oxidase with insulin secretion, the study of potential changes induced by the supplementation with ω-3 FA on the superoxide (O2•) content, and expression of NAD(P)H oxidase subunits, becomes of great importance for a better understanding of the pancreatic β cells physiology. In this study, the group supplemented with ω-3 FA showed a significant reduction in the O2• content in the presence of 5.6 and 16.7mM glucose. Moreover, ω-3 FA supplementation reduced the expression of NAD(P)H oxidase subunits, and increased the expression of the antioxidant enzyme superoxide dismutase (SOD 1 and 2). Although still unknown, the mechanism that decreased the content of reactive oxygen species (ROS) of the pancreatic islets of animals subjected to daily intake of fish oil is relevant, because it represents an improved regulation of the redox state during GSIS.

Suplementação alimentar com óleo de peixe reduz a expressão da NADPH oxidase e aumenta a expressão da SOD1 e SOD2 em ilhotas pancreáticas de ratos.