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. 2020 Sep 3;10:14531. doi: 10.1038/s41598-020-71475-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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Glycogen accumulation in WT and PFKFB2 KI mice with UUO and FAN. Glycogen increased in both UUO (A) and FAN (B) models in WT and PFKFB2 KI mice. In the FAN model, there was a significant increase in glycogen in the untreated PFKFB2 KI control mice compared to WT and a non-significant trend in the sham-operated UUO mice. In the FAN model, there was a significantly greater increase in PFKFB2 mice with disease compared with WT (B). This did not occur in the UUO mice (A). *P < 0.05, **P < 0.01, ***P < 0.001. Mean + S.D. n = 7 per group.