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• W2019925176 endingPage "E677" @default.
• W2019925176 startingPage "E670" @default.
• W2019925176 abstract "It has long been thought that long-chain free fatty acids (FFAs) stimulate insulin secretion via mechanisms involving their metabolism in pancreatic beta-cells. Recently, it was reported that FFAs function as endogenous ligands for GPR40, a G protein-coupled receptor, to amplify glucose-stimulated insulin secretion in an insulinoma cell line and rat islets. However, signal transduction mechanisms for GPR40 in beta-cells are little known. The present study was aimed at elucidating GPR40-linked Ca(2+) signaling mechanisms in rat pancreatic beta-cells. We employed oleic acid (OA), an FFA that has a high affinity for the rat GPR40, and examined its effect on cytosolic Ca(2+) concentration ([Ca(2+)](i)) in single beta-cells by fura 2 fluorescence imaging. OA at 1-10 microM concentration-dependently increased [Ca(2+)](i) in the presence of 5.6, 8.3, and 11.2 mM, but not 2.8 mM, glucose. OA-induced [Ca(2+)](i) increases at 11.2 mM glucose were inhibited in beta-cells transfected with small interfering RNA targeted to rat GPR40 mRNA. OA-induced [Ca(2+)](i) increases were also inhibited by phospholipase C (PLC) inhibitors, U73122 and neomycin, Ca(2+)-free conditions, and an L-type Ca(2+) channel blocker, nitrendipine. Furthermore, OA increased insulin release from isolated islets at 8.3 mM glucose, and it was markedly attenuated by PLC and L-type Ca(2+) channel inhibitors. These results demonstrate that OA interacts with GPR40 to increase [Ca(2+)](i) via PLC- and L-type Ca(2+) channel-mediated pathway in rat islet beta-cells, which may be link to insulin release." @default.
• W2019925176 created "2016-06-24" @default.
• W2019925176 creator A5000201507 @default.
• W2019925176 creator A5005250441 @default.
• W2019925176 creator A5021448631 @default.
• W2019925176 date "2005-10-01" @default.
• W2019925176 modified "2023-09-25" @default.
• W2019925176 title "Oleic acid interacts with GPR40 to induce Ca²⁺signaling in rat islet β-cells: mediation by PLC and L-type Ca²⁺channel and link to insulin release" @default.
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• W2019925176 doi "https://doi.org/10.1152/ajpendo.00035.2005" @default.
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