title: Measures of oxidized low-density lipoprotein and oxidative stress are not related and not elevated in otherwise healthy men with the metabolic syndrome.
abstract: OBJECTIVE
  The metabolic syndrome predisposes to the development of cardiovascular diseases. Oxidative stress and elevated circulating oxidized low-density lipoprotein (LDL) concentrations are related to cardiovascular disease and proposed to be features of the metabolic syndrome. F2-isoprostanes are lipid peroxidation products and considered the most reliable biomarkers of oxidative stress.
  
  
  RESULTS
  Plasma oxidized LDL (oxLDL) and urinary 8-iso-prostaglandin F2alpha (8-iso-PGF2alpha; the major F2-isoprostane) were analyzed in a cross-sectional study of 289 healthy men (62 to 64 years of age). Individuals completed a 7-day dietary record, and fasting plasma insulin, lipid, and lipoprotein concentrations, LDL particle size, and inflammatory markers were determined. National Cholesterol Education Program/Adult Treatment Panel III (NCEP/ATPIII) criteria were used to define the metabolic syndrome and individuals were grouped according to the number of risk factors for the metabolic syndrome (0, [n=88; 30%]; > or =1, [n=179; 62%], metabolic syndrome [n=22; 8%]). Group comparisons revealed no differences for oxLDL, 8-iso-PGF2alpha, or reported intake of macronutrients, whereas C-reactive protein and interleukin-6 were increased in the metabolic syndrome. LDL cholesterol strongly determined oxLDL in univariate and multivariate analysis, but no relationship to 8-iso-PGF2alpha was found. In turn, 8-iso-PGF2alpha was related to reported intake of fat, fatty acids, and dietary antioxidants.
  
  
  CONCLUSIONS
  There were no increases in plasma oxLDL or measures of oxidative stress (urinary 8-iso-PGF2alpha) in these otherwise healthy 63-year-old men with the metabolic syndrome. Furthermore, no relationship between oxLDL and 8-iso-PGF2alpha was found, but our results suggest a role for dietary factors in oxidative stress.
authors.affiliation: Department of Medicine, Karolinska Institutet, Sweden. per.sjogren@ki.se
authors.forename: Per
authors.initials: P
authors.lastname: Sjogren
authors.forename: Samar
authors.initials: S
authors.lastname: Basu
authors.forename: Magdalena
authors.initials: M
authors.lastname: Rosell
authors.forename: Angela
authors.initials: A
authors.lastname: Silveira
authors.forename: Ulf
authors.initials: U
authors.lastname: de Faire
authors.forename: Bengt
authors.initials: B
authors.lastname: Vessby
authors.forename: Anders
authors.initials: A
authors.lastname: Hamsten
authors.forename: Mai-Lis
authors.initials: ML
authors.lastname: Hellenius
authors.forename: Rachel M
authors.initials: RM
authors.lastname: Fisher
mesh_terms: D050197:Atherosclerosis / Q000178:diet therapy / Q000453:epidemiology / Q000378:metabolism*; D015237:Dinoprost / Q000031:analogs & derivatives / Q000652:urine; D005247:Feeding Behavior; D006801:Humans; D008077:Lipoproteins, LDL / Q000097:blood*; D008297:Male; D024821:Metabolic Syndrome / Q000178:diet therapy / Q000453:epidemiology / Q000378:metabolism*; D008875:Middle Aged; D015999:Multivariate Analysis; D015596:Nutrition Assessment; D018384:Oxidative Stress / Q000502:physiology*; D012307:Risk Factors
chemical_list: D008077:Lipoproteins, LDL; C099252:oxidized low density lipoprotein; C075750:8-epi-prostaglandin F2alpha; D015237:Dinoprost