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• W2078954719 abstract "The aim of this study was to investigate the extent to which inflammation is linked with plasma endothelial lipase (EL) concentrations among healthy sedentary men. Plasma C-reactive protein (CRP) concentrations were measured with a highly sensitive commercial immunoassay, plasma interleukin-6 (IL-6) concentrations were measured using a commercial ELISA, and plasma secretory phospholipase A2 type IIA (sPLA2-IIA) concentrations were measured using a commercial assay in a sample of 74 moderately obese men (mean body mass index, 29.8 ± 5.2 kg/m2). Plasma EL concentrations were positively correlated with various indices of obesity, fasting plasma insulin, and plasma CRP, IL-6, and sPLA2-IIA concentrations. Multiple regression analyses revealed that plasma CRP concentrations explained 14.5% (P = 0.0008) of the variance in EL concentrations. When entered into the model, LPL activity accounted for 16.1% (P < 0.0001) and plasma CRP concentrations accounted for 20.9% (P < 0.0001) of the variance in EL concentrations. The combined impact of visceral adipose tissue (VAT) and of an inflammation score on EL concentrations was investigated. Among subjects with high or low VAT, those having a high inflammation score based on plasma CRP, IL-6, and sPLA2-IIA concentrations had increased plasma EL concentrations (P = 0.0005). In conclusion, our data reveal a strong association between proinflammatory cytokines and plasma EL concentrations among healthy people with low or high VAT levels. The aim of this study was to investigate the extent to which inflammation is linked with plasma endothelial lipase (EL) concentrations among healthy sedentary men. Plasma C-reactive protein (CRP) concentrations were measured with a highly sensitive commercial immunoassay, plasma interleukin-6 (IL-6) concentrations were measured using a commercial ELISA, and plasma secretory phospholipase A2 type IIA (sPLA2-IIA) concentrations were measured using a commercial assay in a sample of 74 moderately obese men (mean body mass index, 29.8 ± 5.2 kg/m2). Plasma EL concentrations were positively correlated with various indices of obesity, fasting plasma insulin, and plasma CRP, IL-6, and sPLA2-IIA concentrations. Multiple regression analyses revealed that plasma CRP concentrations explained 14.5% (P = 0.0008) of the variance in EL concentrations. When entered into the model, LPL activity accounted for 16.1% (P < 0.0001) and plasma CRP concentrations accounted for 20.9% (P < 0.0001) of the variance in EL concentrations. The combined impact of visceral adipose tissue (VAT) and of an inflammation score on EL concentrations was investigated. Among subjects with high or low VAT, those having a high inflammation score based on plasma CRP, IL-6, and sPLA2-IIA concentrations had increased plasma EL concentrations (P = 0.0005). In conclusion, our data reveal a strong association between proinflammatory cytokines and plasma EL concentrations among healthy people with low or high VAT levels. Endothelial lipase (EL) is the most recently discovered member of the lipase gene family (1Jaye M. Lynch K.J. Krawiec T. Marchadier D. Maugeais C. Doan K. South V. Amin D. Perrone M. Rader D.J. A novel endothelial-derived lipase that modulates HDL metabolism..Nat. Genet. 1999; 21: 424-428Crossref PubMed Scopus (416) Google Scholar, 2Hirata K. Dichek H.L. Cioffi J.A. Choi S.Y. Leeper N.J. Quintana L. Kronmal G.S. Cooper A.D. Quertermous T. Cloning of a unique lipase from endothelial cells extends the lipase gene family..J. Biol. Chem. 1999; 274: 14170-14175Abstract Full Text Full Text PDF PubMed Scopus (262) Google Scholar), which also includes LPL and HL. Whereas EL acts mainly as a phospholipase, it also contributes to the hydrolysis of triglyceride to a lesser extent (3McCoy M.G. Sun G.S. Marchadier D. Maugeais C. Glick J.M. Rader D.J. Characterization of the lipolytic activity of endothelial lipase..J. Lipid Res. 2002; 43: 921-929Abstract Full Text Full Text PDF PubMed Google Scholar). Recent studies have suggested that EL is an important modulator of HDL concentrations (4Maugeais C. Tietge U.J. Broedl U.C. Marchadier D. Cain W. McCoy M.G. Lund-Katz S. Glick J.M. Rader D.J. Dose-dependent acceleration of high-density lipoprotein catabolism by endothelial lipase..Circulation. 2003; 108: 2121-2126Crossref PubMed Scopus (130) Google Scholar). It has also been shown that EL was more effective at hydrolyzing lipids in the HDL range ex vivo (3McCoy M.G. Sun G.S. Marchadier D. Maugeais C. Glick J.M. Rader D.J. Characterization of the lipolytic activity of endothelial lipase..J. Lipid Res. 2002; 43: 921-929Abstract Full Text Full Text PDF PubMed Google Scholar). A few studies have recently suggested a potential role of EL in modulating lipoprotein metabolism in proinflammatory states, such as atherosclerosis. Indeed, Hirata et al. (5Hirata K. Ishida T. Matsushita H. Tsao P.S. Quertermous T. Regulated expression of endothelial cell-derived lipase..Biochem. Biophys. Res. Commun. 2000; 272: 90-93Crossref PubMed Scopus (82) Google Scholar) first showed that EL mRNA concentrations in cells were upregulated by inflammatory cytokines implicated in vascular diseases, such as tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β). Jin et al. (6Jin W. Sun G.S. Marchadier D. Octtaviani E. Glick J.M. Rader D.J. Endothelial cells secrete triglyceride lipase and phospholipase activities in response to cytokines as a result of endothelial lipase..Circ. Res. 2003; 92: 644-650Crossref PubMed Scopus (106) Google Scholar) have demonstrated that the triglyceride lipase and phospholipase activities of endothelial cells in response to cytokines were primarily the result of the upregulation of EL expression. In a lipopolysaccharide-induced mouse model of inflammation, EL mRNA and protein concentrations were markedly increased in aorta, lung, heart, kidney, liver, and spleen. This upregulation in mouse tissues was accompanied by an increased EL activity in postheparin plasma (7Kojima Y. Hirata K. Ishida T. Shimokawa Y. Inoue N. Kawashima S. Quertermous T. Yokoyama M. Endothelial lipase modulates monocyte adhesion to the vessel wall: a potential role in inflammation..J. Biol. Chem. 2004; 279: 54032-54038Abstract Full Text Full Text PDF PubMed Scopus (50) Google Scholar). In vitro data have suggested that EL may also promote monocyte adhesion to the vascular endothelium through an interaction with heparan sulfate proteoglycans (7Kojima Y. Hirata K. Ishida T. Shimokawa Y. Inoue N. Kawashima S. Quertermous T. Yokoyama M. Endothelial lipase modulates monocyte adhesion to the vessel wall: a potential role in inflammation..J. Biol. Chem. 2004; 279: 54032-54038Abstract Full Text Full Text PDF PubMed Scopus (50) Google Scholar). This upregulation of EL by proinflammatory cytokines contrasts with the downregulated LPL (8Feingold K.R. Marshall M. Gulli R. Moser A.H. Grunfeld C. Effect of endotoxin and cytokines on lipoprotein lipase activity in mice..Arterioscler. Thromb. 1994; 14: 1866-1872Crossref PubMed Google Scholar) and HL (9Feingold K.R. Memon R.A. Moser A.H. Shigenaga J.K. Grunfeld C. Endotoxin and interleukin-1 decrease hepatic lipase mRNA levels..Atherosclerosis. 1999; 142: 379-387Abstract Full Text Full Text PDF PubMed Scopus (49) Google Scholar) activity in vivo in response to acute chronic inflammation.Badellino and colleagues (10Badellino K.O. Wolfe M.L. Reilly M.P. Rader D.J. Endothelial lipase concentrations are increased in metabolic syndrome and associated with increased coronary atherosclerosis..PLoS Medicine. 2005; 3: 245-252Crossref Scopus (148) Google Scholar) recently observed in the large Study of Inherited Risk of Atherosclerosis that plasma EL concentrations in both preheparin and postheparin plasma significantly correlated with all National Cholesterol Education Program Adult Treatment Panel III-defined metabolic syndrome factors, including body mass index, and with subclinical atherosclerosis. More recent data from our group have revealed a significant positive correlation between plasma EL concentrations and visceral fat accumulation. However, our analysis indicated that this association was most likely mediated by other factors, because the level of expression of EL in visceral adipose tissue was extremely low (11Paradis M.E. Badellino K.O. Rader D.J. Tchernof A. Richard C. Luu-The V. Deshaies Y. Bergeron J. Archer R. Couture P. et al.Visceral adiposity and endothelial lipase..J. Clin. Endocrinol. Metab. 2006; 91: 3538-3543Crossref PubMed Scopus (35) Google Scholar). Because in vitro and animal studies have observed increased EL concentrations in response to inflammation, we sought to investigate whether the proatherogenic effects of EL could be linked to inflammation and to examine the extent to which proinflammatory status could explain, at least partly, the association between visceral fat and plasma EL concentrations. Thus, the aim of this study was to further investigate how inflammation is associated with plasma EL concentrations among healthy sedentary men with various amounts of visceral adipose tissue.MATERIALS AND METHODSSubjectsA sample of 80 sedentary men was recruited through the media in the Québec City metropolitan area. Individuals with endocrine, cardiovascular, hepatic, and renal disorders as well as those using medication affecting lipid metabolism, smokers, individuals with excessive alcohol intake, and those with unstable weight within the year preceding the study were excluded from the study. Subjects having plasma C-reactive protein (CRP) concentrations > 10 mg/l, plasma secretory phospholipase A2 type IIA (sPLA2-IIA) concentrations > 900 ng/dl, plasma IL-6 concentrations > 10 mg/l, and those without sPLA2-IIA values were not included in this analysis (n = 6). Thus, analyses were conducted in a sample of 74 men. Similar results were obtained when these subjects were included in the analyses. Each participant signed a consent form approved by the Clinical Research Ethics Committee of Laval University.Anthropometrics and body composition measurementsBody weight and waist circumference were measured according to standardized procedures (12Lohman T. Roche A. Martorel R. Anthropometric standardization reference manual.in: In The Airlie (VA) Consensus Conference. Human Kinetics Books, Champaign, IL1988: 39-80Google Scholar). Total, subcutaneous, and visceral adipose tissue (VAT) accumulation were assessed by computed tomography as described previously (11Paradis M.E. Badellino K.O. Rader D.J. Tchernof A. Richard C. Luu-The V. Deshaies Y. Bergeron J. Archer R. Couture P. et al.Visceral adiposity and endothelial lipase..J. Clin. Endocrinol. Metab. 2006; 91: 3538-3543Crossref PubMed Scopus (35) Google Scholar).Laboratory methodsBlood samples were collected after a 12 h fast. Samples were then immediately centrifuged at 4°C for 10 min at 1,500 g and stored at 4°C until processed. Plasma lipid and apolipoprotein concentrations were measured according to standardized procedures as detailed elsewhere (13Landry N. Bergeron N. Archer R. Samson P. Corneau L. Bergeron J. Deriaz O. Whole-body fat oxidation rate and plasma triacylglycerol concentrations in men consuming an ad libitum high-carbohydrate or low-carbohydrate diet..Am. J. Clin. Nutr. 2003; 77: 580-586Crossref PubMed Scopus (23) Google Scholar). Fasting plasma glucose concentrations were determined with a glucose oxidase assay from Sigma (St. Louis, MO) (14Raabo E. Terkildsen T. On the enzymatic determination of blood glucose..Scand. J. Clin. Lab. Invest. 1960; 12: 402-407Crossref PubMed Scopus (594) Google Scholar). Plasma insulin concentrations were measured by a commercial double-antibody radioimmunoassay (Linco, St. Louis, MO), which shows essentially no cross-reaction with proinsulin (15Despres J.P. Lamarche B. Mauriege P. Cantin B. Dagenais G.R. Moorjani S. Lupien P.J. Hyperinsulinemia as an independent risk factor for ischemic heart disease..N. Engl. J. Med. 1996; 334: 952-957Crossref PubMed Scopus (1618) Google Scholar). Distinct subpopulations of LDL particles were separated in whole plasma using nondenaturing 2–16% gradient gel electrophoresis as described previously (16St. Pierre A.C. Ruel I.L. Cantin B. Dagenais G.R. Bernard P.M. Despres J.P. Lamarche B. Comparison of various electrophoretic characteristics of LDL particles and their relationship to the risk of ischemic heart disease..Circulation. 2001; 104: 2295-2299Crossref PubMed Scopus (224) Google Scholar). Oxidized LDL concentrations were measured using a commercial ELISA according to the manufacturer's instructions (Alpco Diagnostics, Windham, NH). CRP concentrations were measured with a highly sensitive commercial immunoassay (Dade Behring, Mississauga, Ontario, Canada) as described previously (17Pirro M. Bergeron J. Dagenais G.R. Bernard P.M. Cantin B. Despres J.P. Lamarche B. Age and duration of follow-up as modulators of the risk for ischemic heart disease associated with high plasma C-reactive protein levels in men..Arch. Intern. Med. 2001; 161: 2474-2480Crossref PubMed Scopus (120) Google Scholar). Plasma IL-6 concentrations were measured in samples using a commercially available ELISA (R&D Systems, Minneapolis, MN) (18St. Pierre A.C. Cantin B. Bergeron J. Pirro M. Dagenais G.R. Despres J.P. Lamarche B. Inflammatory markers and long-term risk of ischemic heart disease in men A 13-year follow-up of the Quebec Cardiovascular Study..Atherosclerosis. 2005; 182: 315-321Abstract Full Text Full Text PDF PubMed Scopus (63) Google Scholar). Plasma TNFα concentrations were measured with a commercial ELISA (R&D Systems, Abingdon, Oxon, UK).Plasma postheparin (60 IU/kg body weight) LPL and HL activities as well as EL mass were measured after a 12 h overnight fast. LPL and HL activities were determined in postheparin plasma after preincubation with SDS (19Bower J.F. Deshaies Y. Pfeifer M. Tanenberg R.J. Barakat H.A. Ethnic differences in postprandial triglyceride response to a fatty meal and lipoprotein lipase in lean and obese African American and Caucasian women..Metabolism. 2002; 51: 211-217Abstract Full Text PDF PubMed Scopus (34) Google Scholar), as described previously by Watson et al. (20Watson T.D. Tan C.E. McConnell M. Clegg S.K. Squires L.F. Packard C.J. Measurement and physiological significance of lipoprotein and hepatic lipase activities in preheparin plasma..Clin. Chem. 1995; 41: 405-412Crossref PubMed Scopus (35) Google Scholar). Activities were expressed as micromoles of free fatty acids released per milliliter of plasma per hour. Postheparin plasma EL concentrations were measured by an ELISA using a polyclonal antibody (10Badellino K.O. Wolfe M.L. Reilly M.P. Rader D.J. Endothelial lipase concentrations are increased in metabolic syndrome and associated with increased coronary atherosclerosis..PLoS Medicine. 2005; 3: 245-252Crossref Scopus (148) Google Scholar). The intra-assay variability was 6.8%, and the interassay variability was 10.3%. Plasma concentrations of sPLA2-IIA were measured using a commercial assay according to the manufacturer's procedure (Cayman Chemical, Ann Arbor, MI). This is an ELISA system with a monoclonal antibody for capture and a polyclonal antibody with colorimetric detection. The coefficient of variation for the determination of sPLA2-IIA was 7%.Statistical analysisData were analyzed using SAS (version 8.2; SAS Institute, Cary, NC). Spearman's correlation coefficients were calculated to investigate the associations between plasma EL concentrations and inflammatory markers. Stepwise and multiple linear regression analyses were used to identify independent correlates of plasma EL concentrations. In the first model, the contributions of plasma CRP, IL-6, and sPLA2-IIA were investigated. In the second model, LPL and HL activities, VAT area, age, and plasma apolipoprotein B concentrations were added to the model. An inflammation score ranging from 0 to 6 was defined using predefined values of plasma CRP [group 1, ⩽1 mg/l; group 2, >1 mg/l and ⩽3 mg/l; and group 3, >3 mg/l (21Pearson T.A. Mensah G.A. Alexander R.W. Anderson J.L. Cannon III, R.O. Criqui M. Fadl Y.Y. Fortmann S.P. Hong Y. Myers G.L. et al.Markers of inflammation and cardiovascular disease: application to clinical and public health practice. A statement for healthcare professionals from the Centers for Disease Control and Prevention and the American Heart Association..Circulation. 2003; 107: 499-511Crossref PubMed Scopus (5102) Google Scholar)], IL-6 (first tertile, ⩽1.3 mg/l; second tertile, >1.3 mg/l and ⩽1.8 mg/l; and third tertile, >1.8 mg/l), and sPLA2-IIA (first tertile, ⩽105.1 ng/dl; second tertile, >105.1 ng/dl and ⩽154.4 ng/dl; and third tertile, >154.4 ng/dl). For each variable, 0 point was attributed to those in the first group or tertile, 1 point was given to those in the second group or tertile, and 2 points were given to those in the top group or tertile. The inflammation score was arbitrarily categorized as low (<3 points) and high (⩾3 points). Subgroups of subjects with high or low VAT were arbitrarily defined using the median of the distribution (142 cm2). The presence of the metabolic syndrome was determined using the National Cholesterol Education Program Adult Treatment Panel III definition (22Expert Panel. 2001. Executive summary of the third report of the National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III). J. Am. Med. Assoc.285: 2486–2497.Google Scholar). Differences in plasma EL concentrations between the different subgroups were assessed by ANOVA. Pairwise comparisons among groups were performed using the post-hoc Duncan multiple range test. P < 0.01 was used for statistical significance.RESULTSMen investigated in this study (n = 74) were between 20.1 and 56.2 years of age and were overweight as a group, with a mean body mass index of 29.8 ± 5.2 kg/m2 (Table 1 ). They had a relatively normal plasma lipid profile as a group, with mean plasma LDL-cholesterol, triglycerides, and HDL-cholesterol concentrations of 3.00 ± 0.88, 1.45 ± 0.71, and 1.04 ± 0.18 mmol/l, respectively. Plasma EL concentrations were not normally distributed and ranged from 122 to 2,703 ng/ml.TABLE 1Characteristics of men (n = 74)CharacteristicMean ± SDRangeAge (years)37.9 ± 11.720.1–56.2Body mass index (kg/m2)29.8 ± 5.220.1–45.0Waist circumferencean = 72. (cm)99.1 ± 14.869.0–134.0Visceral adipose tissue (cm2)149.2 ± 80.224.4–323.8Total cholesterol (mmol/l)4.55 ± 1.022.03–6.71LDL-cholesterol (mmol/l)3.00 ± 0.880.97–5.19HDL-cholesterol (mmol/l)1.04 ± 0.180.64–1.52Triglycerides (mmol/l)1.45 ± 0.710.45–4.06Apolipoprotein B (g/l)0.99 ± 0.260.40–1.50LDL peak particle size (Å)257.3 ± 5.7245.8–269.5ELbEL concentrations in postheparin plasma are presented as geometric means ± SD. (ng/ml)866.4 ± 1.9122.0–2703.0EL, endothelial lipase.a n = 72.b EL concentrations in postheparin plasma are presented as geometric means ± SD. Open table in a new tab Plasma EL concentrations were positively correlated with VAT, fasting plasma insulin, CRP, IL-6, sPLA2-IIA, total cholesterol, total triglycerides, total apolipoprotein B, apolipoprotein C-III, LDL-cholesterol, and LDL-apolipoprotein B concentrations and were negatively correlated with postheparin plasma LPL activity among this sample of men when adjusted for age (Table 2 ). Similar results were obtained when correlations were not adjusted for age (data not shown). As shown in Fig. 1 , plasma EL concentrations were significantly increased with inflammation. Plasma TNF-α did not correlate with plasma EL concentrations (r = −0.10, P = 0.54; data not shown) and therefore was not included in the inflammation score.TABLE 2Spearman correlation with plasma EL concentrations (n = 74)VariablerPTotal cholesterol (mmol/l)0.370.001Triglycerides (mmol/l)0.370.001Apolipoprotein B (g/l)0.330.005Apolipoprotein C-III (g/l)0.320.006HDL-cholesterol (mmol/l)0.0060.96LDL-cholesterol (mmol/l)0.300.01LDL-apolipoprotein B (g/l)0.290.01Oxidized LDL (U/l)an = 56.0.230.08Visceral adipose tissue area (cm2)0.350.003Fasting insulin (pmol/l)0.400.0005Fasting glucose (mmol/l)0.120.31IL-6 (mg/l)0.330.004CRP (mg/l)0.350.003sPLA2-IIA (ng/dl)0.420.0002LPL activity (μmol FFA/ml/h)bn = 72.−0.370.002HL activity (μmol FFA/ml/h)bn = 72.0.170.15CRP, C-reactive protein; IL-6, interleukin-6; sPLA2-IIA, secretory phospholipase A2 type IIA. r indicates partial correlations adjusted for age.a n = 56.b n = 72. Open table in a new tab Multiple regression analyses were undertaken to distinguish the contribution of various inflammation variables to the variance in EL concentrations. The first model included only variables related to inflammation. As presented in Table 3 , plasma CRP concentrations explained 14.5% (P = 0.0008) of the variance in plasma EL concentrations. When entered into the model, LPL activity accounted for 16.1% (P < 0.0001) and plasma CRP concentrations accounted for 20.9% (P < 0.0001) of the variance in EL concentrations (model 2). Plasma IL-6 concentrations did not contribute to the variance in plasma EL concentrations in this multivariate model. In the third model, the inflammation score explained 26.6% (P < 0.0001) of the variance in plasma EL concentrations, whereas LPL activity contributed to 13.5% (P = 0.0002) of this variation. These contributions were independent of age, VAT, and apolipoprotein B concentrations.TABLE 3Multivariate regression analyses showing the independent contributions of inflammation to plasma EL concentrationsDependant Variable: ELModelIndependent VariablesPartial R2 ×100PModel 1CRP14.50.0008sPLA2-IIA5.90.02IL-6—0.27Model 2CRP20.9<0.0001LPL activity16.1<0.0001sPLA2-IIA5.80.01HL activity2.70.07Visceral adipose tissue—0.44Age—0.57Apolipoprotein B—0.50IL-6—0.87Model 3Inflammation score26.6<0.0001LPL activity13.50.0002HL activity—0.12Visceral adipose tissue Age—0.13Apolipoprotein B—0.33—0.21Plasma EL, CRP, IL-6, and sPLA2-IIA concentrations and LPL and HL activities were log10-transformed before analysis. Open table in a new tab Subjects with and without the metabolic syndrome were divided arbitrarily into two groups based on the CRP value of 1 mg/l. Figure 2A shows that among men with the metabolic syndrome, those having higher plasma CRP concentrations had the highest plasma EL concentrations, and these concentrations were significantly different from those of men without the metabolic syndrome and with low plasma CRP concentrations. Men without the metabolic syndrome but with high plasma CRP concentrations and men with the metabolic syndrome with low plasma CRP concentrations had intermediate plasma EL concentrations. We then looked at plasma EL concentrations according to the inflammation score among subjects with and without the metabolic syndrome. Figure 2B shows that among men with high inflammation scores, plasma EL concentrations were comparably increased in the absence and presence of the metabolic syndrome.Fig. 2.Influence of inflammation on plasma EL concentrations among men with and without the metabolic syndrome. The metabolic syndrome was present when three or more of the criteria established by the National Cholesterol Education Program Adult Treatment Panel III were met. A: The CRP value of 1 mg/l was used to classify subjects with low or high plasma CRP concentrations. B: The inflammation score based on CRP, IL-6, and sPLA2-IIA has been described in Materials and Methods. Plasma EL concentrations are presented as geometric means ± SD. The P values shown refer to the trend for the stepwise increasing bars performed on log10-transformed plasma EL values adjusted for age. The pairwise comparison between each group was achieved using the post-hoc Duncan multiple range test. Significant differences with the corresponding group are indicated above the bars.View Large Image Figure ViewerDownload Hi-res image Download (PPT)It has been shown previously that obesity was associated with plasma EL concentrations among humans (10Badellino K.O. Wolfe M.L. Reilly M.P. Rader D.J. Endothelial lipase concentrations are increased in metabolic syndrome and associated with increased coronary atherosclerosis..PLoS Medicine. 2005; 3: 245-252Crossref Scopus (148) Google Scholar, 11Paradis M.E. Badellino K.O. Rader D.J. Tchernof A. Richard C. Luu-The V. Deshaies Y. Bergeron J. Archer R. Couture P. et al.Visceral adiposity and endothelial lipase..J. Clin. Endocrinol. Metab. 2006; 91: 3538-3543Crossref PubMed Scopus (35) Google Scholar). We hypothesized that the increase in plasma EL concentrations in obesity may be attributable to the presence of a concomitant proinflammatory state. The combined impact of VAT and the inflammation score on EL concentrations was thus investigated by dividing participants on the basis of the median of the distribution of VAT (⩽142 cm2 or >142 cm2). Figure 3 shows that subjects with a high inflammation score, irrespective of their VAT amount, had the highest plasma EL concentrations.Fig. 3.Combined impact of inflammation and visceral adipose tissue (VAT) on plasma EL concentrations. The median value (142 cm2) was used to classify subjects with low or high VAT. See Materials and Methods for a description of the inflammation score based on CRP, IL-6, and sPLA2-IIA concentrations. Plasma EL concentrations are presented as geometric means ± SD. The P value shown refers to the trend for the stepwise increasing bars performed on log10-transformed plasma EL values. Significant differences with the corresponding group are indicated above the bars.View Large Image Figure ViewerDownload Hi-res image Download (PPT)DISCUSSIONOur data in overweight sedentary men suggest that there is a relatively strong association between plasma concentrations of proinflammatory cytokines such as CRP and IL-6 and postheparin plasma EL concentrations. Multivariate analyses revealed that plasma LPL activity and plasma CRP concentrations were the strongest correlates of plasma EL concentrations when taken separately. However, an inflammation score based on plasma CRP, IL-6, and sPLA2-IIA concentrations was the strongest multivariate correlate of plasma EL concentrations. Men with the metabolic syndrome and those without the metabolic syndrome but with a high inflammation score had increased plasma EL concentrations compared with men without the metabolic syndrome and with a low inflammatory score.The positive association between plasma EL concentrations and proinflammatory cytokines such as CRP and IL-6 has never been observed previously among humans. This supports previous studies in which cytokines have been shown to upregulate EL mRNA concentrations in endothelial cells (5Hirata K. Ishida T. Matsushita H. Tsao P.S. Quertermous T. Regulated expression of endothelial cell-derived lipase..Biochem. Biophys. Res. Commun. 2000; 272: 90-93Crossref PubMed Scopus (82) Google Scholar, 6Jin W. Sun G.S. Marchadier D. Octtaviani E. Glick J.M. Rader D.J. Endothelial cells secrete triglyceride lipase and phospholipase activities in response to cytokines as a result of endothelial lipase..Circ. Res. 2003; 92: 644-650Crossref PubMed Scopus (106) Google Scholar) and in a mouse model of inflammation induced by lipopolysaccharide injection (7Kojima Y. Hirata K. Ishida T. Shimokawa Y. Inoue N. Kawashima S. Quertermous T. Yokoyama M. Endothelial lipase modulates monocyte adhesion to the vessel wall: a potential role in inflammation..J. Biol. Chem. 2004; 279: 54032-54038Abstract Full Text Full Text PDF PubMed Scopus (50) Google Scholar). The inverse correlation between LPL activity and EL concentration was unexpected. We hypothesize that it could be partly explained by their common but inverse association with plasma cytokine concentrations. Plasma EL concentrations were also positively correlated with apolipoprotein C-III concentration, which is known to be a natural inhibitor of intravascular LPL activity. Interestingly, the correlation between EL and apolipoprotein C-III concentrations remained significant after adjustment for cytokine concentrations (data not shown). Future studies are needed to investigate this finding.Obesity is characterized by a chronic, systemic, low-grade state of inflammation, as reflected by increased plasma concentrations of CRP and IL-6 (23Yudkin J.S. Stehouwer C.D. Emeis J.J. Coppack S.W. C-reactive protein in healthy subjects: associations with obesity, insulin resistance, and endothelial dysfunction. A potential role for cytokines originating from adipose tissue?.Arterioscler. Thromb. Vasc. Biol. 1999; 19: 972-978Crossref PubMed Scopus (2133) Google Scholar). VAT has also been associated with increased plasma concentrations of CRP (24Lemieux I. Pascot A. Prud'homme D. Almeras N. Bogaty P. Nadeau A. Bergeron J. Despres J.P. Elevated C-reactive protein: another component of the atherothrombotic profile of abdominal obesity..Arterioscler. Thromb. Vasc. Biol. 2001; 21: 961-967Crossref PubMed Scopus (490) Google Scholar). It is now clear that the adipocyte is an active participant in the generation of the inflammatory state in obesity. Adipocytes express a variety of cytokines, including IL-6 (25Fried S.K. Bunkin D.A. Greenberg A.S. Omental and subcutaneous adipose tissues of obese subjects release interleukin-6: depot difference and regulation by glucocorticoid..J. Clin. Endocrinol. Metab. 1998; 83: 847-850Crossref PubMed Scopus (1411) Google S" @default.
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• W2078954719 date "2006-12-01" @default.
• W2078954719 modified "2023-10-02" @default.
• W2078954719 title "Endothelial lipase is associated with inflammation in humans" @default.
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