“…This plasma assay takes advantage of the specificity of HL, EL, and LPL as SN1 lipases; the negligible phospholipase activity of LPL; and the inhibition of EL, but not HL, by high salt. The increased EL phospholipase activity observed in CKD subjects is in agreement with increased mass of EL reported by Fujii et al 18 in CKD patients with low serum albumin or high CRP.…”
Section: Discussionsupporting
confidence: 91%
“…Several studies, both in culture 40 and humans 33 have reported direct association between EL and markers of inflammation, even independent of the degree of abdominal obesity. Fujii et al 18 found that serum EL levels were significantly correlated with tumor necrosis factor-α and hs-CRP in CKD patients; it is suggested that serum EL levels may be elevated in many dialysis patients Values are expressed as r (P values). BMI indicates body mass index; total-C, total cholesterol; HDL-C, high density lipoprotein-cholesterol; LDL-C, low density lipoprotein-cholesterol; apoA-I, apolipoprotein A-I; apoB, apolipoprotein B; HOMA-IR, homeostasis model assessment for insulin resistance index; hs-CRP, high-sensitivity C-reactive protein; HL, hepatic lipase; EL, endothelial lipase.…”
Section: Discussionmentioning
confidence: 99%
“…6 The overexpression of EL results in reduced HDL-C and apolipoprotein A-I (apoA-I) in mice 16 and is inversely correlated with HDL-C in humans. 17 In the only study of EL in HD patients, Fujii et al 18 found that serum EL concentration was significantly higher and HDL-C levels were lower in CKD patients with low serum albumin and high C-reactive protein (CRP) levels, than in those without these abnormalities. Although EL mass has been determined in some studies, to our knowledge EL activity has not been analyzed.…”
Objective—
A novel phospholipase assay was used to measure for the first time the behavior of endothelial and hepatic phospholipase activities in postheparin human plasma of hemodialyzed patients and its relationship with atherogenic and antiatherogenic lipoprotein levels.
Methods and Results—
Endothelial and hepatic phospholipase activity was assessed in a total SN1-specific phospholipase assay, using (1-decanoylthio-1-deoxy-2-decanoyl-sn-glycero-3-phosphoryl) ethylene glycol as the substrate. Hemodialyzed patients presented lower values of total and hepatic phospholipase activity than controls: 4.4 (1.9–9.0) versus 7.5 (3.6–18.0) and 2.6 (0.7–6.2) versus 6.6 (1.3–15.2) μmol of fatty acid released per milliliter of postheparin plasma per hour, respectively (
P
<0.001); however, endothelial lipase (EL) phospholipase activity was increased in patients: 1.7 (0.8–3.0) versus 1.1 (0.1–2.7) μmol of fatty acid released per milliliter of postheparin plasma per hour (
P
=0.008). EL was negatively associated with high-density lipoprotein (HDL)-cholesterol (
r
=–0.427;
P
=0.001), and apolipoprotein A-I levels, total phospholipase, and hepatic lipase activity were directly associated with low-density lipoprotein-cholesterol and apolipoprotein B. The association of EL and HDL-cholesterol remained significant when adjusting for waist circumference (β=–0.26;
P
=0.05), and the effect of hepatic lipase on low-density lipoprotein-cholesterol continued after adjusting for age (β=0.46;
P
= 0.001).
Conclusion—
Our results support the hypothesis that EL is the predominant enzyme responsible for lipolytic catabolism of HDLs in hemodialyzed patients and resolve the apparent paradox observed between low hepatic lipase activity and decreased HDL-cholesterol levels observed in these patients. In addition, the ability to assess total hepatic lipase and EL phospholipase activity in plasma will increase our knowledge of the mechanisms involved in controlling HDL levels and cardiovascular risk in hemodialyzed patients, as well as other populations with low levels of HDL-cholesterol.
“…This plasma assay takes advantage of the specificity of HL, EL, and LPL as SN1 lipases; the negligible phospholipase activity of LPL; and the inhibition of EL, but not HL, by high salt. The increased EL phospholipase activity observed in CKD subjects is in agreement with increased mass of EL reported by Fujii et al 18 in CKD patients with low serum albumin or high CRP.…”
Section: Discussionsupporting
confidence: 91%
“…Several studies, both in culture 40 and humans 33 have reported direct association between EL and markers of inflammation, even independent of the degree of abdominal obesity. Fujii et al 18 found that serum EL levels were significantly correlated with tumor necrosis factor-α and hs-CRP in CKD patients; it is suggested that serum EL levels may be elevated in many dialysis patients Values are expressed as r (P values). BMI indicates body mass index; total-C, total cholesterol; HDL-C, high density lipoprotein-cholesterol; LDL-C, low density lipoprotein-cholesterol; apoA-I, apolipoprotein A-I; apoB, apolipoprotein B; HOMA-IR, homeostasis model assessment for insulin resistance index; hs-CRP, high-sensitivity C-reactive protein; HL, hepatic lipase; EL, endothelial lipase.…”
Section: Discussionmentioning
confidence: 99%
“…6 The overexpression of EL results in reduced HDL-C and apolipoprotein A-I (apoA-I) in mice 16 and is inversely correlated with HDL-C in humans. 17 In the only study of EL in HD patients, Fujii et al 18 found that serum EL concentration was significantly higher and HDL-C levels were lower in CKD patients with low serum albumin and high C-reactive protein (CRP) levels, than in those without these abnormalities. Although EL mass has been determined in some studies, to our knowledge EL activity has not been analyzed.…”
Objective—
A novel phospholipase assay was used to measure for the first time the behavior of endothelial and hepatic phospholipase activities in postheparin human plasma of hemodialyzed patients and its relationship with atherogenic and antiatherogenic lipoprotein levels.
Methods and Results—
Endothelial and hepatic phospholipase activity was assessed in a total SN1-specific phospholipase assay, using (1-decanoylthio-1-deoxy-2-decanoyl-sn-glycero-3-phosphoryl) ethylene glycol as the substrate. Hemodialyzed patients presented lower values of total and hepatic phospholipase activity than controls: 4.4 (1.9–9.0) versus 7.5 (3.6–18.0) and 2.6 (0.7–6.2) versus 6.6 (1.3–15.2) μmol of fatty acid released per milliliter of postheparin plasma per hour, respectively (
P
<0.001); however, endothelial lipase (EL) phospholipase activity was increased in patients: 1.7 (0.8–3.0) versus 1.1 (0.1–2.7) μmol of fatty acid released per milliliter of postheparin plasma per hour (
P
=0.008). EL was negatively associated with high-density lipoprotein (HDL)-cholesterol (
r
=–0.427;
P
=0.001), and apolipoprotein A-I levels, total phospholipase, and hepatic lipase activity were directly associated with low-density lipoprotein-cholesterol and apolipoprotein B. The association of EL and HDL-cholesterol remained significant when adjusting for waist circumference (β=–0.26;
P
=0.05), and the effect of hepatic lipase on low-density lipoprotein-cholesterol continued after adjusting for age (β=0.46;
P
= 0.001).
Conclusion—
Our results support the hypothesis that EL is the predominant enzyme responsible for lipolytic catabolism of HDLs in hemodialyzed patients and resolve the apparent paradox observed between low hepatic lipase activity and decreased HDL-cholesterol levels observed in these patients. In addition, the ability to assess total hepatic lipase and EL phospholipase activity in plasma will increase our knowledge of the mechanisms involved in controlling HDL levels and cardiovascular risk in hemodialyzed patients, as well as other populations with low levels of HDL-cholesterol.
“…Positive associations with total cholesterol, LDL-cholesterol and triglycerides are in accordance with previous findings 8 . However, a strong positive association of EL with HDL-cholesterol-, THDL-p- and SHDL-p- concentrations was in sharp contrast to previous studies reporting either no 7, 23 or a negative association of EL with HDL-cholesterol- and HDL-p- plasma concentrations 8, 15–17 . A possible explanation for this finding might be that the observed relationship does not reflect the enzyme-substrate interaction but rather a concomitant regulation of EL- and HDL- levels into the same direction by the underlying AHF pathophysiology.…”
We hypothesised that the established association of endothelial lipase (EL) plasma levels with atherogenic lipid profile is altered in acute heart failure (AHF) and additionally affected by overlapping metabolic syndrome (MetS). We examined the association of EL plasma levels and lipid/lipoprotein plasma levels in AHF patients without and with overlapping MetS. The study was performed as a single-centre, observational study on 152 AHF patients, out of which 85 had overlapping MetS. In the no-MetS group, EL plasma levels were significantly positively correlated with plasma levels of atherogenic lipids/lipoproteins, including total cholesterol, low-density lipoprotein (LDL)-cholesterol, total LDL particles and triglycerides, but also with plasma levels of antiatherogenic high-density lipoprotein (HDL)-cholesterol, total HDL particles and small HDL particles. In the MetS group, EL plasma levels were positively correlated with triglyceride and small LDL-particle levels, and significantly negatively correlated with plasma levels of large HDL particles as well as with LDL- and HDL-particle size, respectively. EL- and lipid/lipoprotein- plasma levels were different in the no-MetS patients, compared to MetS patients. The association of EL with atherogenic lipid profile is altered in AHF and additionally modified by MetS, which strongly modulates EL- and lipid/lipoprotein-plasma levels in AHF.
“…The lack of association between EL plasma levels and that of inflammatory markers might reflect the impact of gender and age, factors known to modulate plasma levels of inflammatory molecules [6,7]. The lack of significant correlation between plasma EL and HDL levels might be due to medication [8-12] and is in line with a previous report [13]. We concluded that increased EL plasma levels, independent of markers of inflammation or HDL plasma levels, reflect the patients’ overall susceptibility for cerebrovascular events.…”
BackgroundEndothelial lipase (EL) is a phospholipase expressed predominantly by vascular endothelial cells. The goal of the present study was to examine whether EL plasma levels in patients with carotid artery stenosis differ between those with previous history of neurological impairment and those without neurological symptoms.MethodsEL plasma levels were measured by a competitive ELISA assay.ResultsEL plasma levels were significantly higher in the symptomatic, compared with the asymptomatic group (mean 489.61 ± 145 ng/ml (n = 31) vs. 388.39 ± 133 ng/ml (n = 24), t-test, P = 0.011).ConclusionWe concluded that increased EL plasma levels reflect the patients' overall susceptibility for cerebrovascular events.KeywordsAtherosclerosis; Carotid artery stenosis; Endothelial lipase; Neurological impairment; Carotid endarterectomy
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