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Am J Physiol Endocrinol Metab (May 24, 2005). doi:10.1152/ajpendo.00035.2005
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Submitted on January 27, 2005
Accepted on May 11, 2005

Oleic acid interacts with GPR40 to induce Ca2+ signaling in rat islet {beta}-cells: mediation by phospholipase C- and L-type Ca2+ channel and link to insulin release

Ken Fujiwara1, Fumihiko Maekawa1, and Toshihiko Yada1*

1 Department of Physiology, Division of Integrative Physiology, Jichi Medical School, Minamikawachi, Tochigi, Japan

* To whom correspondence should be addressed. E-mail: tyada{at}jichi.ac.jp.

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 Ca2+ signaling mechanisms in rat pancreatic {beta}-cells. We employed oleic acid (OA), a FFA that has a high affinity for the rat GPR40, and examined its effect on cytosolic Ca2+ concentration ([Ca2+]i) in single {beta}-cells by fura-2 fluorescence imaging. OA at 1-10 mM concentration-dependently increased [Ca2+]i in the presence of 5.6, 8.3 and 11.2 mM, but not 2.8 mM, glucose. OA-induced [Ca2+]i increases at 11.2 mM glucose were inhibited in {beta}-cells transfected with small interfering RNA targeted to rat GPR40 mRNA. OA-induced [Ca2+]i increases were also inhibited by phospholipase C (PLC) inhibitors, U73122 and neomycin, Ca2+-free conditions, and an L-type Ca2+ 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 Ca2+ channel inhibitors. These results demonstrate that OA interacts with GPR40 to increase [Ca2+]i via PLC- and L-type Ca2+ channel-mediated pathway in rat islet {beta}-cells, which may be link to insulin release.




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