title: Endothelial lipase activity predicts high-density lipoprotein catabolism in hemodialysis: novel phospholipase assay in postheparin human plasma.
abstract: 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.
  
  
  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).
  
  
  CONCLUSIONS
  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.
authors.affiliation: Laboratory of Lipids and Lipoproteins, Department of Clinical Biochemistry, Faculty of Pharmacy and Biochemistry, University of Buenos Aires, Buenos Aires, Argentina.
authors.forename: Veronica
authors.initials: V
authors.lastname: Miksztowicz
authors.forename: Mary G
authors.initials: MG
authors.lastname: McCoy
authors.forename: Laura
authors.initials: L
authors.lastname: Schreier
authors.forename: Leonardo
authors.initials: L
authors.lastname: Cacciagiú
authors.forename: Alicia
authors.initials: A
authors.lastname: Elbert
authors.forename: Ana Inés
authors.initials: AI
authors.lastname: Gonzalez
authors.forename: Jeffrey
authors.initials: J
authors.lastname: Billheimer
authors.forename: Patrick
authors.initials: P
authors.lastname: Eacho
authors.forename: Daniel J
authors.initials: DJ
authors.lastname: Rader
authors.forename: Gabriela
authors.initials: G
authors.lastname: Berg
mesh_terms: D000328:Adult; D000375:Aging / Q000378:metabolism; D015415:Biomarkers / Q000097:blood; D016022:Case-Control Studies; D008076:Cholesterol, HDL / Q000378:metabolism*; D057075:Enzyme Assays / Q000379:methods*; D005260:Female; D006801:Humans; D007676:Kidney Failure, Chronic / Q000378:metabolism* / Q000503:physiopathology / Q000628:therapy*; D008049:Lipase / Q000097:blood*; D008297:Male; D008875:Middle Aged; D010740:Phospholipases / Q000097:blood; D011237:Predictive Value of Tests; D012044:Regression Analysis; D006435:Renal Dialysis; D055105:Waist Circumference / Q000502:physiology
chemical_list: D015415:Biomarkers; D008076:Cholesterol, HDL; C504173:LIPC protein, human; D010740:Phospholipases; C410382:LIPG protein, human; D008049:Lipase