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. 2022 Sep 24;13(9):817. doi: 10.1038/s41419-022-05259-w

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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 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. 3 — A During resting, approximately 2–5% of cellular glucose enters the hexosamine biosynthesis pathway (HBP) to generate the end product UDP-GlcNAc. B During adaptation, high glucose induces genome instability through O-linked-N-acetylglucosaminylation (O-GlcNAcylation) of phosphofructokinase 1 (PFK1) and ribonucleotide reductase catalytic subunit M1 (RRM1) to direct glycolysis and the pentose phosphate pathway (PPP) into the HBP. C During hyperproliferation, such as in pancreatic cancer cells, both high glucose and high glutamine are required through overactivation/overexpression of PFK1, shunting glycolysis into the PPP and HBP to generate energy and biosynthesis precursors to meet the needs of cancer cells. G6P glucose 6-phosphate, F6P fructose 6-phosphate, FBP fructose 1,6-phosphate, GFAT glutamine:fructose-6-phosphate amidotransferase, R5P ribose 5-phosphate, PRPP phosphoribosyl pyrophosphate, NDP nucleoside diphosphate, dNDP deoxynucleoside diphosphates, GlcN6P glucosamine-6-phosphate, UDP-GlcNAc uridine diphosphate-N-acetylglucosamine.