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. 2017 Jul 10;14:45. doi: 10.1186/s12986-017-0200-8

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© The Author(s). 2017

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided 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 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.

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Fig. 2 — AMPK is associated with the phosphorylation of ACC and MCD to regulate myocardial energy metabolism. Chronic hyperglycemia activates AMPK, resulting in the phosphorylation of ACC, releasing the inhibitory effect of malonly-CoA on CPT1 and subsequently leading to enhanced entry of FFAs via CPT1 into the mitochondria for beta-oxidation. Abnormally increased beta-oxidation is further accountable for mitochondrial membrane damage through peroxyl radicals. Keys: ACC- acetyl-CoA carboxylase; AMPK- 5’ adenosine monophosphate (AMP)-activated protein kinase; CPT1- carnitine palmitoyltransferase 1; FFA- free fatty acid; MCD- malonyl-CoA decarboxylase