title: n-3 polyunsaturated fatty acid supplementation, monocyte adhesion molecule expression and pro-inflammatory mediators in Type 2 diabetes mellitus.
abstract: OBJECTIVE
  To examine the effect of n-3 polyunsaturated fatty acid supplements on the monocyte surface expression of adhesion molecules involved in proatherogenic monocyte-endothelial interactions, and on pro-inflammatory mediators in Type 2 diabetes mellitus.
  
  
  METHODS
  Twenty-nine subjects with Type 2 diabetes and 21 controls without diabetes were studied. Monocyte expression of leucocyte function-associated antigens 1 and 3, intercellular adhesion molecule-1, and the major histocompatibility complex class II molecule HLA-DR were measured using a laser flow cytometric method. Supplementation with 2.08 g n-3 fatty acids for 21 days was undertaken and measurements repeated. Plasma soluble adhesion molecule concentrations, plasminogen activator inhibitor-1 activity and antigen and pro-inflammatory mediators (cysteinyl leukotriene and monocyte leukotriene B4) were also measured.
  
  
  RESULTS
  Groups did not differ in monocyte expression of adhesion molecules or HLA-DR, or in leukotriene production although plasma soluble adhesion molecule concentrations were higher in the diabetes groups (P<0.05). n-3 fatty acid supplementation influenced neither the expression of these molecules nor plasma soluble adhesion molecule concentrations or leukotriene production.
  
  
  CONCLUSIONS
  This study does not support increased monocyte adhesion molecule expression or abnormal monocyte production of pro-inflammatory mediators as mechanisms for increased atherogenic risk in Type 2 diabetes. Cardioprotective actions of n-3 fatty acids may not be mediated through these mechanisms.
authors.affiliation: Bertram Diabetes Research Unit, Norfolk, UK. mjsampson@paston.co.uk
authors.forename: M J
authors.initials: MJ
authors.lastname: Sampson
authors.forename: I R
authors.initials: IR
authors.lastname: Davies
authors.forename: J C
authors.initials: JC
authors.lastname: Brown
authors.forename: V
authors.initials: V
authors.lastname: Morgan
authors.forename: T
authors.initials: T
authors.lastname: Richardson
authors.forename: A J
authors.initials: AJ
authors.lastname: James
authors.forename: A P
authors.initials: AP
authors.lastname: Sampson
authors.forename: D A
authors.initials: DA
authors.lastname: Hughes
mesh_terms: D001792:Blood Platelets / Q000737:chemistry / Q000378:metabolism; D018968:CD58 Antigens / Q000097:blood*; D003924:Diabetes Mellitus, Type 2 / Q000097:blood / Q000276:immunology* / Q000628:therapy*; D019587:Dietary Supplements; D004739:England; D005230:Fatty Acids, Nonesterified / Q000097:blood; D015525:Fatty Acids, Omega-3 / Q000494:pharmacology / Q000627:therapeutic use*; D006684:HLA-DR Antigens / Q000097:blood; D006801:Humans; D007249:Inflammation; D018799:Intercellular Adhesion Molecule-1 / Q000097:blood*; D007975:Leukotriene B4 / Q000097:blood; D016169:Lymphocyte Function-Associated Antigen-1 / Q000097:blood*; D008297:Male; D008875:Middle Aged; D009000:Monocytes / Q000187:drug effects / Q000276:immunology*; D017395:Plasminogen Activator Inhibitor 1 / Q000097:blood; D012016:Reference Values; D044465:White People
chemical_list: D018968:CD58 Antigens; D005230:Fatty Acids, Nonesterified; D015525:Fatty Acids, Omega-3; D006684:HLA-DR Antigens; D016169:Lymphocyte Function-Associated Antigen-1; D017395:Plasminogen Activator Inhibitor 1; D018799:Intercellular Adhesion Molecule-1; D007975:Leukotriene B4