Lucena Camila F, Roma Leticia P, Graciano Maria Fernanda R, Veras Katherine, Simões Daniel, Curi Rui, Carpinelli Angelo R
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.
Pancreas. 2015 Mar;44(2):287-95. doi: 10.1097/MPA.0000000000000249.
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.
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.
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.
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.
本研究旨在评估补充鱼油(FO)对健康大鼠胰岛氧化还原状态的潜在影响。为了测试这些影响是否归因于二十碳五烯酸和二十二碳六烯酸(ω-3),进行了体外实验。
给大鼠补充FO,并获取胰岛。胰岛还在体外使用棕榈酸(P)或二十碳五烯酸+二十二碳六烯酸(ω-3)进行处理。分析胰岛素分泌(葡萄糖刺激的胰岛素分泌)、葡萄糖氧化、蛋白质表达和超氧化物含量。
FO组超氧化物含量降低。此外,FO降低了NAD(P)H氧化酶亚基的表达并增加了超氧化物歧化酶,而未改变β细胞功能。棕榈酸增加了β细胞活性氧(ROS)的产生、细胞凋亡并损害了葡萄糖刺激的胰岛素分泌。在这些条件下,ω-3引发了由P诱导的ROS产生和β细胞凋亡的平行减少,并防止了葡萄糖刺激的胰岛素分泌受损。线粒体ROS产生没有差异。
我们的结果表明,ω-3可保护胰岛免受P诱导的改变。体内补充FO可调节胰腺β细胞的氧化还原状态。鉴于体外效应不涉及线粒体超氧化物的产生,我们可以推测这种保护可能涉及NAD(P)H氧化酶活性。