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. 2020 Apr 28;12:59. doi: 10.1186/s13148-020-00848-y

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© The Author(s) 2020

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. 4 — Hyperglycaemia may affect ten-eleven translocation (TET) and Jumonji C (JmjC) activity by altering Fe²⁺ availability. a Hyperglycaemia increases flux through the polyol pathway, which consumes reduced nicotinamide adenine dinucleotide phosphate (NADPH). Reduced glutathione (GSH) and vitamin C levels may decrease as a result, decreasing the regeneration of Fe²⁺ which is required by TET and JmjC enzymes. Increased generation of reactive oxygen species (ROS) in hyperglycaemia may also affect Fe²⁺ regeneration. b An increase in cyclic adenosine monophosphate (cAMP) levels in hyperglycaemia may increase the intracellular labile Fe²⁺ pool and thus increase TET and JmjC activity. Abbreviations: glucose-6-phosphate (G6P), fructose-6-phosphate (F6P), Fructose-1,6-bisphosphate (F1,6P2), glyceraldehyde-3-phosphate (G3P), 1,3-bisphosphoglycerate (1,3 BPG)