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Lipids in Health and Disease

2015 
Background: It has been observed that ras-transformed cell lines in culture have a higher phosphatidylcholine (PC) biosynthesis rate as well as higher PC-degradation rate (increased PCturnover) than normal cells. In correspondence to these findings, the concentrations of the PCdegradation product lyso-phosphatidylcholine (LPC) in cancer patients were found to be decreased. Our objective was the systematic investigation of the relationship between LPC and inflammatory and nutritional parameters in cancer patients. Therefore, plasma LPC concentrations were assessed in 59 cancer patients and related to nutritional and inflammatory parameters. To determine LPC in blood plasma we developed and validated a HPTLC method. Results: Average plasma LPC concentration was 207 ± 59 μM which corresponds to the lower limit of the reported range in healthy subjects. No correlation between LPC and age, performance status, body mass index (BMI) or fat mass could be seen. However, LPC correlated inversely with plasma C-reactive protein (CRP) and whole blood hydrogen peroxides (HPO). Further, a negative correlation could be observed between LPC and whole body extra cellular fluid volume (ECF) as well as with relative change in body weight since cancer diagnosis. Conclusion: In conclusion, LPC concentrations were decreased in cancer patients. LPC plasma concentrations correlated with weight loss and inflammatory parameters and, therefore, might be a general indicator of severity of malignant disease. Background Phosphatidylcholine (PC), a glycerophospholipid bearing a polar phosphocholine head group and two nonpolar fatty acid hydrocarbon chains, represents the main membrane-forming phospholipid in mammalian cells. Removal of one of the fatty acids, enzymatically or by spontaneous hydrolysis, results in lyso-phosphatidylcholine (LPC). In contrast to PC, which is a membrane forming phospholipid, LPC exerts a lytic action on membranes [1]. In living cells, LPC usually results from membrane PC through the enzymatic action of a phospholipase A2 (PLA2), which cleaves the fatty acid from the 2-position of the glycerol backbone. In the blood, LPC is usually generated by PLA2 or by the lecithin-cholesterol-acyl-transferase Published: 10 July 2007 Lipids in Health and Disease 2007, 6:17 doi:10.1186/1476-511X-6-17 Received: 29 May 2007 Accepted: 10 July 2007 This article is available from: http://www.lipidworld.com/content/6/1/17 © 2007 Taylor 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 cited.
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