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. 2021 Jul 6;11:17. doi: 10.1186/s13395-021-00274-5

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© The Author(s) 2021

Open AccessThis 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/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 7 — Transcriptomic analyses exhibited that the amiloride treatment improved glycolysis and ketone body oxidation in cachetic gastrocnemius. a Heat-map plot of relative transcription levels of muscular atrophy-related genes (n = 4). b Expressions of ACOT1, CD36, OXCT1, BDH2, and ACAT1 proteins. c Quantification of the expressed proteins (n = 4). Statistical significances: p > 0.05, NS; p < 0.05, *; p < 0.01, **; p < 0.001, ***; p < 0.0001, ****. NOR, C57BL/6 or BALB/c normal control mice; CAC, CT26/LLC cachexia mice; AM, amiloride-treated mice; KD, mice inoculated with Rab27-knockdown CT26/LLC cells; ACOT1, acyl-coenzyme A thioesterase 1; CD36, fatty acid translocase; OXCT1, 3-oxoacid CoA transferase 1; BDH2, 3-hydroxybutyrate dehydrogenase 2; ACAT1, acetyl coenzyme A acetyltransferase 1