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. 2016 Jun 10;8:64. doi: 10.1186/s13073-016-0318-8

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© The Author(s). 2016

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. 4 — Metabolic alterations identified in the IT phase of chronic HBV. Increased levels of DHAP-derived plasmalogen phospholipid species, free fatty acids, and acyl carnitines were found. A significant decrease in glycerophospholipids, triglycerides, and sphingomyelins was found, suggesting the HBV hijacking of the cytosolic glycerol-3-phosphate dehydrogenase (GPDH) enzyme, favoring the synthesis of plasmalogen lipid species. Detected metabolic species are highlighted in red with the arrow indicating its trend. DHAP dihydroxyacetone phosphate, G3P glycerol-3-phosphate, LPA lysophosphatidic acid, PA phosphatidic acid, DG diacylglycerol, PE phosphatidylethanolamine, PC phosphatidylcholine, LPE lysophosphatidylethanolamine, LPC lysophosphatidylcholine, TG triglyceride, FFA free fatty acids, pPE plasmalogen phosphatidylethanolamine, pPC plasmalogen phosphatidylcholine, pLPE plasmalogen lysophosphatidylethanolamine, pLPC plasmalogen lysophosphatidylcholine, GAPDH glyceraldehyde-3-phosphate dehydrogenase, TPI triosephosphate isomerase, cGPDH cytosolic glycerol-3-phosphate dehydrogenase, mGPDH mitochondrial glycerol-3-phosphate dehydrogenase