全部 标题 作者
关键词 摘要

OALib Journal期刊
ISSN: 2333-9721
费用:99美元

查看量下载量

相关文章

更多...
PLOS ONE  2014 

Glycerophospholipid and Sphingolipid Species and Mortality: The Ludwigshafen Risk and Cardiovascular Health (LURIC) Study

DOI: 10.1371/journal.pone.0085724

Full-Text   Cite this paper   Add to My Lib

Abstract:

Vascular and metabolic diseases cause half of total mortality in Europe. New prognostic markers would provide a valuable tool to improve outcome. First evidence supports the usefulness of plasma lipid species as easily accessible markers for certain diseases. Here we analyzed association of plasma lipid species with mortality in the Ludwigshafen Risk and Cardiovascular Health (LURIC) study. Plasma lipid species were quantified by electrospray ionization tandem mass spectrometry and Cox proportional hazards regression was applied to assess their association with total and cardiovascular mortality. Overall no differences were detected between total and cardiovascular mortality. Highly polyunsaturated phosphatidylcholine species together with lysophosphatidylcholine species and long chain saturated sphingomyelin and ceramide species seem to be associated with a protective effect. The predominantly circulating phosphatidylcholine-based as well as phosphatidylethanolamine-based ether species and phosphatidylethanolamine species were positively associated with total and cardiovascular mortality. Saturated and monounsaturated phosphatidylcholine species, especially phosphatidylcholine 32:0 (most probably dipalmitoyl-phosphatidylcholine) and palmitate containing sphingomyelin and ceramide species showed together with 24:1 containing sphingomyelin and ceramide species strongest positive association with mortality. A quotient of the sums of the six most protective species and the six species with the strongest positive mortality association indicated an almost 3-fold increased risk of mortality, which was higher than the hazard ratio for known risk factors in our cohort. Plasma lipid species levels and especially ratios of certain species may be valuable prognostic marker for cardiovascular and total mortality.

References

[1]  Scarborough P, Bhatnagar P, Wickramasinghe K, Smolina K, Mitchell C, et al.. (2010) Coronary heart disease statistics 2010 edition. BHF Coronary heart disease statistics at www heartstats org.
[2]  Chavez JA, Summers SA (2010) Lipid oversupply, selective insulin resistance, and lipotoxicity: molecular mechanisms. Biochim Biophys Acta 1801: 252–265.
[3]  Quehenberger O, Armando AM, Brown AH, Milne SB, Myers DS, et al. (2010) Lipidomics reveals a remarkable diversity of lipids in human plasma. J Lipid Res 51: 3299–3305.
[4]  Sorensen CM, Ding J, Zhang Q, Alquier T, Zhao R, et al. (2010) Perturbations in the lipid profile of individuals with newly diagnosed type 1 diabetes mellitus: lipidomics analysis of a Diabetes Antibody Standardization Program sample subset. Clin Biochem 43: 948–956.
[5]  Oresic M, Hyotylainen T, Kotronen A, Gopalacharyulu P, Nygren H, et al.. (2013) Prediction of non-alcoholic fatty-liver disease and liver fat content by serum molecular lipids. Diabetologia.
[6]  Han X, Rozen S, Boyle SH, Hellegers C, Cheng H, et al. (2011) Metabolomics in early Alzheimer's disease: identification of altered plasma sphingolipidome using shotgun lipidomics. PLoS One 6: e21643.
[7]  Sysi-Aho M, Koikkalainen J, Seppanen-Laakso T, Kaartinen M, Kuusisto J, et al. (2011) Serum lipidomics meets cardiac magnetic resonance imaging: profiling of subjects at risk of dilated cardiomyopathy. PLoS One 6: e15744.
[8]  Butler PL, Mallampalli RK (2010) Cross-talk between remodeling and de novo pathways maintains phospholipid balance through ubiquitination. J Biol Chem 285: 6246–6258.
[9]  Schmitz G, Ruebsaamen K (2010) Metabolism and atherogenic disease association of lysophosphatidylcholine. Atherosclerosis 208: 10–18.
[10]  Goncalves I, Edsfeldt A, Ko NY, Grufman H, Berg K, et al. (2012) Evidence supporting a key role of Lp-PLA2-generated lysophosphatidylcholine in human atherosclerotic plaque inflammation. Arterioscler Thromb Vasc Biol 32: 1505–1512.
[11]  Hu C, Kong H, Qu F, Li Y, Yu Z, et al. (2011) Application of plasma lipidomics in studying the response of patients with essential hypertension to antihypertensive drug therapy. Mol Biosyst 7: 3271–3279.
[12]  Graessler J, Schwudke D, Schwarz PE, Herzog R, Shevchenko A, et al. (2009) Top-down lipidomics reveals ether lipid deficiency in blood plasma of hypertensive patients. PLoS One 4: e6261.
[13]  Gieger C, Geistlinger L, Altmaier E, Hrabe de AM, Kronenberg F, et al. (2008) Genetics meets metabolomics: a genome-wide association study of metabolite profiles in human serum. PLoS Genet 4: e1000282.
[14]  Hicks AA, Pramstaller PP, Johansson A, Vitart V, Rudan I, et al. (2009) Genetic determinants of circulating sphingolipid concentrations in European populations. PLoS Genet 5: e1000672.
[15]  Illig T, Gieger C, Zhai G, Romisch-Margl W, Wang-Sattler R, et al. (2010) A genome-wide perspective of genetic variation in human metabolism. Nat Genet 42: 137–141.
[16]  Kopf T, Peer M, Schmitz G (2012) Genetic and Metabolic Determinants of Fatty Acid Chain Length and Desaturation, Their Incorporation into Lipid Classes and Their Effects on Risk of Vascular and Metabolic Disease. In: Suhre K, editors. Genetics Meets Metabolomics. Springer New York. pp. 191–231.
[17]  Pewzner-Jung Y, Ben-Dor S, Futerman AH (2006) When do Lasses (longevity assurance genes) become CerS (ceramide synthases)?: Insights into the regulation of ceramide synthesis. J Biol Chem 281: 25001–25005.
[18]  Zheng W, Kollmeyer J, Symolon H, Momin A, Munter E, et al. (2006) Ceramides and other bioactive sphingolipid backbones in health and disease: lipidomic analysis, metabolism and roles in membrane structure, dynamics, signaling and autophagy. Biochim Biophys Acta 1758: 1864–1884.
[19]  Li X, Becker KA, Zhang Y (2010) Ceramide in redox signaling and cardiovascular diseases. Cell Physiol Biochem 26: 41–48.
[20]  Riboni L, Viani P, Bassi R, Prinetti A, Tettamanti G (1997) The role of sphingolipids in the process of signal transduction. Prog Lipid Res 36: 153–195.
[21]  Maedler K, Spinas GA, Dyntar D, Moritz W, Kaiser N, et al. (2001) Distinct effects of saturated and monounsaturated fatty acids on beta-cell turnover and function. Diabetes 50: 69–76.
[22]  Paumen MB, Ishida Y, Muramatsu M, Yamamoto M, Honjo T (1997) Inhibition of carnitine palmitoyltransferase I augments sphingolipid synthesis and palmitate-induced apoptosis. J Biol Chem 272: 3324–3329.
[23]  Shimabukuro M, Zhou YT, Levi M, Unger RH (1998) Fatty acid-induced beta cell apoptosis: a link between obesity and diabetes. Proc Natl Acad Sci U S A 95: 2498–2502.
[24]  Olivetti G, Abbi R, Quaini F, Kajstura J, Cheng W, et al. (1997) Apoptosis in the failing human heart. N Engl J Med 336: 1131–1141.
[25]  Listenberger LL, Ory DS, Schaffer JE (2001) Palmitate-induced apoptosis can occur through a ceramide-independent pathway. J Biol Chem 276: 14890–14895.
[26]  de Mello VDF, Lankinen M, Schwab U, Kolehmainen M, Lehto S, et al. (2009) Link between plasma ceramides, inflammation and insulin resistance: association with serum IL-6 concentration in patients with coronary heart disease. Diabetologia 52: 2612–2615.
[27]  Spijkers LJ, van den Akker RF, Janssen BJ, Debets JJ, De Mey JG, et al. (2011) Hypertension is associated with marked alterations in sphingolipid biology: a potential role for ceramide. PLoS One 6: e21817.
[28]  Jiang XC, Paultre F, Pearson TA, Reed RG, Francis CK, et al. (2000) Plasma sphingomyelin level as a risk factor for coronary artery disease. Arterioscler Thromb Vasc Biol 20: 2614–2618.
[29]  Pilz S, Scharnagl H, Tiran B, Seelhorst U, Wellnitz B, et al. (2006) Free fatty acids are independently associated with all-cause and cardiovascular mortality in subjects with coronary artery disease. J Clin Endocrinol Metab 91: 2542–2547.
[30]  Pilz S, Scharnagl H, Tiran B, Wellnitz B, Seelhorst U, et al. (2007) Elevated plasma free fatty acids predict sudden cardiac death: a 6.85-year follow-up of 3315 patients after coronary angiography. Eur Heart J 28: 2763–2769.
[31]  Winkelmann BR, Marz W, Boehm BO, Zotz R, Hager J, et al. (2001) Rationale and design of the LURIC study–a resource for functional genomics, pharmacogenomics and long-term prognosis of cardiovascular disease. Pharmacogenomics 2: S1–73.
[32]  Kleber ME, Grammer TB, Renner W, Marz W (2010) Effect of the rs2259816 polymorphism in the HNF1A gene on circulating levels of c-reactive protein and coronary artery disease (the ludwigshafen risk and cardiovascular health study). BMC Med Genet 11: 157.
[33]  Stojakovic T, Scharnagl H, Trauner M, Pieske B, Wellnitz B, et al. (2010) Serum gamma-glutamyl transferase and mortality in persons undergoing coronary angiography-The Ludwigshafen Risk and Cardiovascular Health Study. Atherosclerosis 208: 564–571.
[34]  Liebisch G, Lieser B, Rahtenberg J, Drobnik W, Schmitz G (2005) High-throughput quantification of phosphatidylcholine and sphingomyelin by electrospray ionization tandem mass spectrometry coupled with isotope corrections algorithim (vol 1686, pg 108, 2004). Biochimica et Biophysica Acta-Molecular and Cell Biology of Lipids 1734: 86–89.
[35]  Liebisch G, Drobnik W, Reil M, Trumbach B, Arnecke R, et al. (1999) Quantitative measurement of different ceramide species from crude cellular extracts by electrospray ionization tandem mass spectrometry (ESI-MS/MS). J Lipid Res 40: 1539–1546.
[36]  Liebisch G, Drobnik W, Lieser B, Schmitz G (2002) High-throughput quantification of lysophosphatidylcholine by electrospray ionization tandem mass spectrometry. Clin Chem 48: 2217–2224.
[37]  Liebisch G, Vizcaino JA, Koefeler H, Troetzmueller M, Griffiths WJ, et al.. (2013) Shorthand Notation for Lipid Structures Derived from Mass Spectrometry. J Lipid Res.
[38]  Merino DM, Ma DW, Mutch DM (2010) Genetic variation in lipid desaturases and its impact on the development of human disease. Lipids Health Dis 9: 63.
[39]  Ottestad I, Hassani S, Borge GI, Kohler A, Vogt G, et al. (2012) Fish oil supplementation alters the plasma lipidomic profile and increases long-chain PUFAs of phospholipids and triglycerides in healthy subjects. PLoS One 7: e42550.
[40]  Leskinen T, Rinnankoski-Tuikka R, Rintala M, Seppanen-Laakso T, Pollanen E, et al.. (2010) Differences in muscle and adipose tissue gene expression and cardio-metabolic risk factors in the members of physical activity discordant twin pairs. PLoS One 5..
[41]  Lu Y, Vaarhorst A, Merry AH, Dolle ME, Hovenier R, et al. (2012) Markers of endogenous desaturase activity and risk of coronary heart disease in the CAREMA cohort study. PLoS One 7: e41681.
[42]  Barber MN, Risis S, Yang C, Meikle PJ, Staples M, et al. (2012) Plasma lysophosphatidylcholine levels are reduced in obesity and type 2 diabetes. PLoS One 7: e41456.
[43]  Horres CR, Hannun YA (2012) The roles of neutral sphingomyelinases in neurological pathologies. Neurochem Res 37: 1137–1149.
[44]  Duan RD, Bergman T, Xu N, Wu J, Cheng Y, et al. (2003) Identification of human intestinal alkaline sphingomyelinase as a novel ecto-enzyme related to the nucleotide phosphodiesterase family. J Biol Chem 278: 38528–38536.
[45]  Huitema K, van den Dikkenberg J, Brouwers JF, Holthuis JC (2004) Identification of a family of animal sphingomyelin synthases. EMBO J 23: 33–44.

Full-Text

comments powered by Disqus

Contact Us

service@oalib.com

QQ:3279437679

WhatsApp +8615387084133

WeChat 1538708413