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. 2020 Nov 3;10:18879. doi: 10.1038/s41598-020-75306-z

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© The Author(s) 2020

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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/.

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Differences in fecal metabolites between patients and controls, responders and non-responders and the effect of EEN on the fecal metabolome. Panels (A–C) show OPLS-DA plots. This analysis indicates that ¹HNMR analysis can distinguish controls (blue) from patients (red) at T0, panel (A). A marginal EEN induced change in metabolome from T0 (red) to T2 (blue) is shown in panel (B). The difference in metabolome between responders (blue) and non-responders (red) at T0 is shown in panel (C). Panel (D) shows increased total fecal amino acids in patients that decrease during EEN therapy. Panel (E) shows that bile salts are not elevated in patients and unchanged during therapy. Panels (F) and (G) show decreased bile salt metabolism and hydrophobicity in patients at T0 that is partially normalized during therapy. Panels (H) and (I) show increased levels of trimethylamine and cadaverine respectively and show partial normalization of these compounds during EEN therapy. HC healthy controls, R responders, NR non-responders.