Stearidonic acid promotes insulin secretion via stimulation of G protein-coupled receptor 40 in MIN6 pancreatic β-cells. (September 2019)

• Record Type: Journal Article
• Authors: Gao, Yi-Xiong; Fan, Cuihong; Tan, Xin; Zhang, Jian; Wang, Jingzhong
• Is Part Of: Journal of functional foods. Volume 60(2019)
• Publication Date: 2019-09
• Subjects: Stearidonic acid -- G protein-coupled receptor 40 -- Insulin -- N-3 polyunsaturated fatty acid -- MIN6 pancreatic β-cell; ALA alpha linolenic acid -- BSA bovine serum albumin -- DHA docosahexaenoic acid -- DMEM Dulbecco's modified Eagle's medium -- EPA eicosapentaenoic acid -- FAME fatty acid methyl ester -- FBS fetal bovine serum -- GPR40 G protein-coupled receptor 40 -- GSIS glucose-stimulated insulin secretion -- IP3 inositol 1, 4, 5-trisphosphate -- KRBH buffer Krebs-Ringer bicarbonate HEPES buffer -- PA palmitic acid -- PLC phospholipase C -- PUFA polyunsaturated fatty acid -- SDA stearidonic acid -- SFA saturated fatty acid; Functional foods -- Analysis -- Periodicals; Food -- Biotechnology -- Periodicals; Nutrition -- Periodicals; 613.2
• DOI: 10.1016/j.jff.2019.103450
• Languages: English
• ISSNs: 1756-4646

Abstract

Graphical abstract: The insulinotropic effect of stearidonic acid resulted from direct and indirect pathways. The direct promotion resulted from activation of G protein-coupled receptor 40 and its downstream signaling molecules, and the indirect promotion was attributed to antagonistic effects of stearidonic acid on long chain saturated fatty acid-mediated pancreatic β-cells impairment. Highlights: This study found stearidonic acid (SDA) has insulinotropic effect. The expression of GPR40 in MIN6 pancreatic β-cells increased after SDA treatment. The insulinotropic effect of SDA resulted from stimulation of GPR40-related signaling pathway. SDA can antagonize long chain saturated fatty acid-mediated pancreatic β-cells impairment. Abstract: 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).