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. 2014 Feb 12;11:10. doi: 10.1186/1743-7075-11-10

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Copyright © 2014 Zhang et al.; licensee BioMed Central Ltd.

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. 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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Transcriptional regulation pathways of PDK4 in different tissues under various nutritional states. Inactivation of PDC by up-regulation of PDK4 can switch glucose catabolism to fatty acid utilization. There are different transcriptional regulation pathways in skeletal muscle, liver, white adipose tissue and heart under various nutritional conditions (energy deprivation, high fat diet consumption, exercise, diseases, drugs). Akt/PKB: protein kinase B; AMPK: 5’-AMP-activated protein kinase; CD36: Cluster of differentiation 36; C/EBPβ: CCAAT/enhancer-binding protein β; eIF4E: Eukaryotic initiation factor 4E; ERRα: Estrogen related receptor α; FAT: Fatty acid transporter; FoxO1: Forkhead box protein O1; LXR: Liver X receptor; MAPK: p38 mitogen-activated protein kinase; PDC: Pyruvate dehydrogenase complex; PDK4: Pyruvate dehydrogenase kinase 4; PGC1α: PPARγ co-activator 1α; PPARs: Peroxisome proliferator-activated receptors; SHP: Small heterodimer partner; STAT5: Signal transducer and activator of transcription 5.