title: Fish-oil supplementation alters numbers of circulating endothelial progenitor cells and microparticles independently of eNOS genotype.
abstract: BACKGROUND
  Emerging cellular markers of endothelial damage and repair include endothelial microparticles (EMPs) and endothelial progenitor cells (EPCs), respectively. Effects of long-chain (LC) n-3 (omega-3) polyunsaturated fatty acids (PUFAs) and the influence of genetic background on these markers are not known.
  
  
  OBJECTIVE
  We investigated effects of fish-oil supplementation on both classical and novel markers of endothelial function in subjects prospectively genotyped for the Asp298 endothelial nitric oxide synthase (eNOS) polymorphism and at moderate risk of cardiovascular disease (CVD).
  
  
  METHODS
  A total of 84 subjects with moderate risk of CVD (GG: n = 40; GT/TT: n = 44) completed a randomized, double-blind, placebo-controlled, 8-wk crossover trial of fish-oil supplementation that provided 1.5 g LC n-3 PUFAs/d. Effects of genotype and fish-oil supplementation on the blood lipid profile, inflammatory markers, vascular function (by using peripheral artery tonometry), and numbers of circulating EPCs and EMPs (by using flow cytometry) were assessed.
  
  
  RESULTS
  There was no significant effect of fish-oil supplementation on blood pressure, plasma lipids, or plasma glucose, although there was a trend (P = 0.069) toward a decrease in the plasma triglyceride concentration after fish-oil supplementation compared with placebo treatment. GT/TT subjects tended to have higher concentrations of total cholesterol and low-density lipoprotein cholesterol, but vascular function was not affected by either treatment or eNOS genotype. Biochemical markers of endothelial function were also unaffected by treatment and eNOS genotype. In contrast, there was a significant effect of fish-oil supplementation on cellular markers of endothelial function. Fish-oil supplementation increased numbers of EPCs and reduced numbers of EMPs relative to those with placebo treatment, which potentially favored the maintenance of endothelial integrity. There was no influence of genotype for any cellular markers of endothelial function, which indicated that effects of fish-oil supplementation were independent of eNOS genotype.
  
  
  CONCLUSIONS
  Emerging cellular markers of endothelial damage, integrity, and repair appear to be sensitive to potentially beneficial modification by dietary n-3 PUFAs. This trial was registered at www.controlled-trials.com/isrctn as ISRCTN76272133.
authors.affiliation: From the Hugh Sinclair Unit of Human Nutrition, Department of Food & Nutritional Sciences and Institute for Cardiovascular and Metabolic Research (S-YW, JM-P, JAL, and PY) and the Department of Mathematics and Statistics (ST), University of Reading, Whiteknights, Reading, United Kingdom.
authors.forename: Szu-Yun
authors.initials: SY
authors.lastname: Wu
authors.affiliation: From the Hugh Sinclair Unit of Human Nutrition, Department of Food & Nutritional Sciences and Institute for Cardiovascular and Metabolic Research (S-YW, JM-P, JAL, and PY) and the Department of Mathematics and Statistics (ST), University of Reading, Whiteknights, Reading, United Kingdom.
authors.forename: Jordi
authors.initials: J
authors.lastname: Mayneris-Perxachs
authors.affiliation: From the Hugh Sinclair Unit of Human Nutrition, Department of Food & Nutritional Sciences and Institute for Cardiovascular and Metabolic Research (S-YW, JM-P, JAL, and PY) and the Department of Mathematics and Statistics (ST), University of Reading, Whiteknights, Reading, United Kingdom.
authors.forename: Julie A
authors.initials: JA
authors.lastname: Lovegrove
authors.affiliation: From the Hugh Sinclair Unit of Human Nutrition, Department of Food & Nutritional Sciences and Institute for Cardiovascular and Metabolic Research (S-YW, JM-P, JAL, and PY) and the Department of Mathematics and Statistics (ST), University of Reading, Whiteknights, Reading, United Kingdom.
authors.forename: Susan
authors.initials: S
authors.lastname: Todd
authors.affiliation: From the Hugh Sinclair Unit of Human Nutrition, Department of Food & Nutritional Sciences and Institute for Cardiovascular and Metabolic Research (S-YW, JM-P, JAL, and PY) and the Department of Mathematics and Statistics (ST), University of Reading, Whiteknights, Reading, United Kingdom.
authors.forename: Parveen
authors.initials: P
authors.lastname: Yaqoob
mesh_terms: D000328:Adult; D000368:Aged; D015415:Biomarkers / Q000097:blood; D001786:Blood Glucose / Q000378:metabolism; D001792:Blood Platelets / Q000378:metabolism; D001794:Blood Pressure / Q000187:drug effects; D002318:Cardiovascular Diseases / Q000235:genetics / Q000517:prevention & control; D055252:Cell-Derived Microparticles / Q000378:metabolism; D008076:Cholesterol, HDL / Q000097:blood; D008078:Cholesterol, LDL / Q000097:blood; D019587:Dietary Supplements; D004311:Double-Blind Method; D066026:Endothelial Progenitor Cells / Q000378:metabolism*; D015525:Fatty Acids, Omega-3 / Q000008:administration & dosage; D005260:Female; D005395:Fish Oils / Q000008:administration & dosage*; D005838:Genotype; D006801:Humans; D008297:Male; D008875:Middle Aged; D052250:Nitric Oxide Synthase Type III / Q000235:genetics*; D011110:Polymorphism, Genetic; D011446:Prospective Studies; D012307:Risk Factors; D014280:Triglycerides / Q000097:blood; D055815:Young Adult
chemical_list: D015415:Biomarkers; D001786:Blood Glucose; D008076:Cholesterol, HDL; D008078:Cholesterol, LDL; D015525:Fatty Acids, Omega-3; D005395:Fish Oils; D014280:Triglycerides; C496314:NOS3 protein, human; D052250:Nitric Oxide Synthase Type III