title: Plasma Lp-PLA(2)  mass and apoB-lipoproteins that carry Lp-PLA(2)  decrease after sodium.
abstract: BACKGROUND
  Lipoprotein-associated phospholipase A(2) (Lp-PLA(2) ) is a novel cardiovascular risk marker, which is predominantly complexed to apolipoprotein (apo) B-containing lipoproteins in human plasma. As increasing dietary sodium intake may decrease plasma apoB-containing lipoproteins, we tested whether a sodium challenge lowers plasma Lp-PLA(2) mass, as well as the levels of apoB-containing lipoprotein particles carrying Lp-PLA(2) (apoB-Lp-PLA(2) ), employing a newly developed enzyme-linked immunosorbent assay.
  
  
  METHODS
  In 45 women and 31 men (mean age 44 ± 14 years), plasma Lp-PLA(2) mass (turbidimetric immunoassay), the level of apoB-Lp-PLA(2) , expressed in apoB concentration and lipoproteins were measured in response to a 3-day challenge with 9 g sodium chloride tablets daily.
  
  
  RESULTS
  Urinary sodium excretion increased from 165 ± 60 to 321 ± 70 mmol/24 h (P<0.001) after salt loading. Plasma Lp-PLA(2) mass decreased from 618 (493-719) to 588 (465-698) μg/L (P<0.001), and apoB-Lp-PLA(2) decreased from 0.276 (0.200-0.351) to 0.256 (0.189-0.328) g LDL protein/L (P=0.004) in response to the sodium challenge together with decreases in plasma total cholesterol, nonhigh-density lipoprotein (HDL) cholesterol, low-density lipoprotein (LDL) cholesterol, apolipoprotein B and the total cholesterol/HDL cholesterol ratio (P<0.01 for all). Changes in plasma Lp-PLA(2) mass were correlated positively with changes in total cholesterol, LDL cholesterol and non-HDL cholesterol (r=0.260-0.276, P<0.05 to P<0.02), whereas changes in apoB-Lp-PLA(2) were correlated positively with changes in non-HDL cholesterol and in the total cholesterol/HDL cholesterol ratio (r=0.232-0.385, P<0.05-0.01).
  
  
  CONCLUSIONS
  Both plasma Lp-PLA(2) mass levels and apoB-Lp-PLA(2) decrease in response to a short-term oral sodium challenge.
authors.affiliation: Department of Endocrinology, University of Groningen and University Medical Center Groningen, Groningen, The Netherlands.
authors.forename: Alexander
authors.initials: A
authors.lastname: Constantinides
authors.forename: Michiel N
authors.initials: MN
authors.lastname: Kerstens
authors.forename: Bert D
authors.initials: BD
authors.lastname: Dikkeschei
authors.forename: L Joost
authors.initials: LJ
authors.lastname: van Pelt
authors.forename: Constantinos C
authors.initials: CC
authors.lastname: Tellis
authors.forename: Alexandros D
authors.initials: AD
authors.lastname: Tselepis
authors.forename: Robin P F
authors.initials: RP
authors.lastname: Dullaart
mesh_terms: D043203:1-Alkyl-2-acetylglycerophosphocholine Esterase / Q000097:blood*; D000328:Adult; D001055:Apolipoproteins B / Q000097:blood*; D002784:Cholesterol / Q000097:blood*; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D012982:Sodium, Dietary / Q000008:administration & dosage / Q000378:metabolism* / Q000652:urine; D014280:Triglycerides / Q000097:blood
chemical_list: D001055:Apolipoproteins B; D012982:Sodium, Dietary; D014280:Triglycerides; D002784:Cholesterol; D043203:1-Alkyl-2-acetylglycerophosphocholine Esterase