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. 2017 Dec 21;7(12):305. doi: 10.1038/s41387-017-0005-x

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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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Fig. 2 — Toxicities of PA, MePA, OA, MeOA and EA (trans-OA) a-b and toxicities of the PUFAs LA (C18:2) and γ-LNA (C18:3) in comparison with the MUFA OA (C18:1) and to PriA in human EndoC-βH1 beta cells and their ability to antagonise the toxic effect of OA (C18:1) c. EndoC-βH1 beta cells were incubated for 2 days with PA, MePA, OA, MeOA and EA (trans-OA)(all FFAs 500 µM). Thereafter, caspase-3 activity a and propidium iodide fluorescence b were measured. In addition, EndoC-βH1 beta cells were incubated for 2 days with the polyunsaturated fatty acids (PUFAs) LA (500 µM), γ-LNA (500 µM), and for comparison with the monounsaturated OA (500 µM), as well as the branched-chain PriA (200 µM). Furthermore, combinations of OA with the PUFAs (500 µM each) were incubated. Thereafter, caspase-3 activity was measured c. Data are means ± SEM of 5–8 independent experiments. **p < 0.01 compared with untreated control cells; ^# p < 0.05, ^## p < 0.01 compared with the corresponding non-methylated fatty acid.