title: Serum paraoxonase-3 concentration is associated with insulin sensitivity in peripheral artery disease and with inflammation in coronary artery disease.
abstract: OBJECTIVE
  There are no data on the relationship between serum paraoxonase-3 (PON3) concentration and atherosclerosis in humans. Our aim was to investigate possible associations, using recently developed methods, in patients with peripheral artery disease (PAD) or coronary artery disease (CAD).
  
  
  METHODS
  We studied 118 PAD and 72 CAD patients and 175 healthy volunteers. Serum PON3 was determined by in-house ELISA using polyclonal antibodies generated against a synthetic peptide with a sequence specific to PON3. Polymorphisms of the PON3 promoter were analysed by the Iplex Gold MassArray™ method.
  
  
  RESULTS
  There was a significant increase in serum PON3 concentration in both groups of patients with respect to the control group. In PAD patients, we observed significant positive correlations between PON3, insulin levels and HOMA index. These associations were not observed in CAD. There were significant positive associations between serum PON3 and β-2-microglobulin, CCL2 and high-sensitivity C-reactive protein in CAD patients, but not in PAD. We did not find any significant differences in PON3 gene promoter polymorphisms and their haplotypes between patients and controls, indicating that associations were not genetically determined.
  
  
  CONCLUSIONS
  In both atherosclerotic phenotypes, serum PON3 concentration was increased, but this was associated with decreased insulin sensitivity in PAD and with inflammation in CAD.
authors.affiliation: Centre de Recerca Biomèdica, Hospital Universitari de Sant Joan, Institut d'Investigació Sanitària Pere Virgili, Universitat Rovira i Virgili, C. Sant Joan s/n, 43201 Reus, Catalonia, Spain.
authors.forename: Anna
authors.initials: A
authors.lastname: Rull
authors.forename: Raúl
authors.initials: R
authors.lastname: García
authors.forename: Laura
authors.initials: L
authors.lastname: Fernández-Sender
authors.forename: Anabel
authors.initials: A
authors.lastname: García-Heredia
authors.forename: Gerard
authors.initials: G
authors.lastname: Aragonès
authors.forename: Raúl
authors.initials: R
authors.lastname: Beltrán-Debón
authors.forename: Judit
authors.initials: J
authors.lastname: Marsillach
authors.forename: Josep M
authors.initials: JM
authors.lastname: Alegret
authors.forename: Vicente
authors.initials: V
authors.lastname: Martín-Paredero
authors.forename: Bharti
authors.initials: B
authors.lastname: Mackness
authors.forename: Michael
authors.initials: M
authors.lastname: Mackness
authors.forename: Jorge
authors.initials: J
authors.lastname: Joven
authors.forename: Jordi
authors.initials: J
authors.lastname: Camps
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D043303:Aryldialkylphosphatase / Q000097:blood* / Q000235:genetics; D015415:Biomarkers / Q000097:blood; D016022:Case-Control Studies; D003324:Coronary Artery Disease / Q000097:blood / Q000201:enzymology* / Q000235:genetics / Q000276:immunology; D003430:Cross-Sectional Studies; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D006239:Haplotypes; D006801:Humans; D007249:Inflammation / Q000097:blood / Q000201:enzymology* / Q000503:physiopathology; D018836:Inflammation Mediators / Q000097:blood; D007333:Insulin Resistance; D015810:Linkage Disequilibrium; D008297:Male; D008875:Middle Aged; D058729:Peripheral Arterial Disease / Q000097:blood / Q000201:enzymology* / Q000235:genetics / Q000503:physiopathology; D010641:Phenotype; D010865:Pilot Projects; D020641:Polymorphism, Single Nucleotide; D011401:Promoter Regions, Genetic; D013030:Spain; D015854:Up-Regulation
chemical_list: D015415:Biomarkers; D018836:Inflammation Mediators; D043303:Aryldialkylphosphatase; C468406:PON1 protein, human; C113656:PON3 protein, human