Stearidonic acid promotes insulin secretion via stimulation of G protein-coupled receptor 40 in MIN6 pancreatic β-cells
Stearidonic acid promotes insulin secretion via stimulation of G protein-coupled receptor 40 in MIN6 pancreatic β-cells
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十八碳四烯酸通过刺激 MIN6 胰腺 β 细胞中的 G 蛋白偶联受体 40 促进胰岛素分泌
DOI：
10.1016/j.jff.2019.103450
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发表时间：
2019-09
影响因子：
5.6
通讯作者：
Yi-Xiong Gao
中科院分区：
文献类型：
--
作者：
Yi-Xiong Gao
本研究旨在探讨十八碳四烯酸（stearidonic acid，SDA）是否具有促胰岛素分泌作用及其作用机制。用SDA处理MIN 6胰腺β细胞并分析效果。SDA处理24 h后，细胞内G蛋白偶联受体40（GPR 40）的蛋白和mRNA表达均增加，而SDA处理组与对照组细胞内SDA成分无统计学差异。细胞内Ca ~（2+）浓度在处理后15 s内升高，但用U-73122（磷脂酶C抑制剂）或BAPTA-AM（Ca ~（2+）螯合剂）预孵育后，细胞内Ca ~（2+）浓度升高被抑制。结果表明，SDA能显著增加胰岛素分泌，SDA加U-73122或BAPTA-AM均能抑制GSIS的分泌。SDA的存在拮抗棕榈酸介导的MIN 6细胞死亡。这些发现首次表明SDA可以通过刺激GPR 40相关信号通路（直接作用）和通过拮抗长链饱和脂肪酸介导的损伤（间接作用）促进胰腺β细胞中的GSIS。
The aim of this study is to research whether stearidonic acid (SDA) has insulinotropic effect and the mechanisms. MIN6 pancreatic β-cells were treated with SDA and effects were analyzed. Protein and mRNA expressions of G protein-coupled receptor 40 (GPR40) increased after 24-h SDA treatment, whereas there was no statistical difference of cellular SDA composition between SDA and control groups. The cytosolic Ca2+ increased in 15 s after treatment, but increment was inhibited when MIN6 cells were preincubated with U-73122 (phospholipase C inhibitor) or BAPTA-AM (Ca2+ chelator). The glucose-stimulated insulin secretion (GSIS) increased after treatment, and GSIS was also inhibited by SDA plus U-73122 or BAPTA-AM. The presence of SDA antagonized palmitic acid-mediated MIN6 cells death. These findings indicate for the first time that SDA can promote GSIS in pancreatic β-cells via stimulation of GPR40-related signaling pathway (direct effect), and via antagonistic effect on long chain saturated fatty acid-mediated impairment (indirect effect).
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