Omega-3 supplementation improves pancreatic islet redox status: in vivo and in vitro studies.

Pancreas

From the *Department of Physiology and Biophysics, Institute of Biomedical Sciences, University of São Paulo, São Paulo, São Paulo; and †Department of Physiology Sciences, University of Londrina, Londrina, Paraná, Brazil.

Published: March 2015

AI Article Synopsis

  • The study aimed to assess how fish oil (FO) supplementation affects the redox status of pancreatic islets in healthy rats, focusing on the roles of specific omega-3 fatty acids.
  • Rats supplemented with FO showed decreased superoxide levels and reduced expression of harmful oxidase subunits, while preserving insulin secretion functions.
  • Omega-3 fatty acids counteracted the negative effects of palmitate on pancreatic β-cells, leading to reduced oxidative stress and improved insulin secretion, suggesting a protective mechanism tied to NAD(P)H oxidase activity.

Article Abstract

Objectives: The aim of the study was to evaluate the potential changes induced by fish oil (FO) supplementation on the redox status of pancreatic islets from healthy rats. To test whether these effects were due to eicosapentaenoic acid and docosahexaenoic acid (ω-3), in vitro experiments were performed.

Methods: Rats were supplemented with FO, and pancreatic islets were obtained. Islets were also treated in vitro with palmitate (P) or eicosapentaenoic acid + docosahexaenoic acid (ω-3). Insulin secretion (GSIS), glucose oxidation, protein expression, and superoxide content were analyzed.

Results: The FO group showed a reduction in superoxide content. Moreover, FO reduced the expression of NAD(P)H oxidase subunits and increased superoxide dismutase, without altering β-cell function. Palmitate increased β-cell reactive oxygen species (ROS) production, apoptosis, and impaired GSIS. Under these conditions, ω-3 triggered a parallel reduction in ROS production and β-cell apoptosis induced by P and protected against the impairment in GSIS. There was no difference in mitochondrial ROS production.

Conclusions: Our results show that ω-3 protect pancreatic islets from alterations induced by P. In vivo FO supplementation modulates the redox state of pancreatic β-cell. Considering that in vitro effects do not involve mitochondrial superoxide production, we can speculate that this protection might involve NAD(P)H oxidase activity.

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Source
http://dx.doi.org/10.1097/MPA.0000000000000249DOI Listing

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