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. 2017 Jul 5;7:4657. doi: 10.1038/s41598-017-04730-5

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© The Author(s) 2017

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Role of FFAR1 and fatty acid β-oxidation in the effect of palmitate on EndoC-βH1 insulin secretion and respiration. Cells were exposed to 5.6 mM glucose in the absence (white symbols) or presence (black symbols) of palmitate with and without ANT825 and/or etomoxir, trimetazidine. Insulin secretion (panel A). Representative kinetic OCR recordings from cells acutely exposed to palmitate with and without ANT825 and/or etomoxir (panel B). Mitochondrial OCR (panel C), ATP-coupled OCR (panel D) and proton leak OCR (panel E). Results show mean ± SEM (panels A,C-E,) (n = 5), and mean ± SD (panel B) (N = 6). *P < 0.05 vs. control, ^#P < 0.05 vs. palmitate alone and ^&P < 0.05 vs. corresponding P-etomoxir/trimetazidine.