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. 2022 May 24;12:8771. doi: 10.1038/s41598-022-12827-9

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© The Author(s) 2022

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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The role of HIF1α in regulating butyrate oxidation. (A) Percent change in oxygen consumption rate (OCR) relative to baseline in which HCT116 and HIF1α KO cells treated with and without butyrate (5 mM). Total contribution of butyrate toward OCR (%) is observed after injection of 2-deoxyglucose (2DG). The right panel shows the area under the curve (AUC) analysis from OCR measurements taken after 2DG injection but before azide injection. These measurements represent butyrate oxidation (arbitrary units). Data points represent the average OCR (%) over 3–5 replicates per condition for butyrate oxidation measurements. (B) Percent change in extracellular acidification rate (ECAR) relative to baseline in which HCT116 and HIF1α KO cells respond to glucose, 2DG, and azide. The right panel shows AUC from ECAR measurements taken after glucose injection but before 2DG injection. These measurements represent glycolysis (arbitrary units). Data points represent the average ECAR (%) over 3–5 replicates per condition for glycolysis measurements. Error bars are mean ± SEM.