title: The inverse relation of HDL anti-oxidative functionality with serum amyloid a is lost in metabolic syndrome subjects.
abstract: OBJECTIVE
  Anti-oxidative properties of high density lipoproteins (HDL) are relevant for atheroprotection. HDL carry serum amyloid A (SAA), which may impair HDL functionality. We questioned whether HDL anti-oxidative capacity is determined by SAA.
  
  
  METHODS
  Relationships of HDL anti-oxidative capacity (% inhibition of low density lipoprotein oxidation in vitro) with SAA were determined in 54 non-diabetic subjects without metabolic syndrome (MetS) and 68 subjects with MetS (including 51 subjects with Type 2 diabetes mellitus).
  
  
  RESULTS
  SAA levels were higher in MetS subjects, coinciding higher high sensitive C-reactive protein (hs-CRP) and lower HDL cholesterol and apolipoprotein (apo) A-I levels (P<0.001 for all). HDL anti-oxidative capacity was not different between subjects with and without MetS (P=0.76), but the HDL anti-oxidation index (HDL anti-oxidative capacity multiplied by individual HDL cholesterol concentrations), as a measure of global anti-oxidative functionality of HDL, was lower in Mets subjects (P<0.001). HDL anti-oxidative capacity was correlated inversely with SAA levels in subjects without MetS (r=-0.286, P=0.036). Notably, this relationship was independent of HDL cholesterol or apoA-I (P<0.05 for both). In contrast, no relation of HDL anti-oxidative capacity with SAA was observed in MetS subjects (r=0.032, P=0.80). The relationship of SAA with HDL anti-oxidative capacity was different in subjects with MetS compared to subjects without MetS (P=0.039 for the interaction between the presence of MetS and SAA on HDL anti-oxidative capacity) taking age and diabetes status into account.
  
  
  CONCLUSIONS
  Higher SAA levels may impair HDL anti-oxidative functionality. The relationship of this physiologically relevant HDL functionality measure with circulating SAA levels is apparently disturbed in metabolic syndrome.
authors: Department of Endocrinology, Center for Liver, Digestive and Metabolic Diseases, University Medical Center Groningen and University of Groningen, Groningen. r.p.f.dullaart@int.umcg.nl
authors: Robin P F
authors: RP
authors: Dullaart
authors: Jan Freark
authors: JF
authors: de Boer
authors: Wijtske
authors: W
authors: Annema
authors: Uwe J F
authors: UJ
authors: Tietge
mesh_terms: D000368:Aged; D000975:Antioxidants / Q000032:analysis*; D016632:Apolipoprotein A-I / Q000097:blood; D015992:Body Mass Index; D002097:C-Reactive Protein / Q000032:analysis / Q000378:metabolism; D008076:Cholesterol, HDL / Q000097:blood*; D003430:Cross-Sectional Studies; D003924:Diabetes Mellitus, Type 2 / Q000097:blood; D005260:Female; D006801:Humans; D016014:Linear Models; D008077:Lipoproteins, LDL / Q000097:blood; D008297:Male; D024821:Metabolic Syndrome / Q000097:blood*; D008875:Middle Aged; D000685:Serum Amyloid A Protein / Q000032:analysis*
chemical_list: D000975:Antioxidants; D016632:Apolipoprotein A-I; D008076:Cholesterol, HDL; D008077:Lipoproteins, LDL; D000685:Serum Amyloid A Protein; C099252:oxidized low density lipoprotein; D002097:C-Reactive Protein