title: Consumption of saturated fat impairs the anti-inflammatory properties of high-density lipoproteins and endothelial function.
abstract: OBJECTIVE
  The purpose of this study was to investigate the influence of dietary fatty acids on the anti-inflammatory properties of high-density lipoproteins (HDL) and vascular function.
  
  
  BACKGROUND
  The effect of dietary fatty acids on atherogenesis remains uncertain.
  
  
  METHODS
  Fourteen adults consumed an isocaloric meal containing either a polyunsaturated or a saturated fat on 2 occasions. The effects of post-prandial HDL on endothelial cell expression of intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) were determined. Flow-mediated dilation (FMD) and microvascular reactivity were assessed before and 3 and 6 h after the meal.
  
  
  RESULTS
  Plasma triglycerides, insulin, and nonesterified fatty acids rose after the meals. The HDL collected 6 h after the saturated meal were less effective than HDL isolated from fasting plasma in terms of their ability to inhibit expression of ICAM-1 and VCAM-1, whereas HDL collected 6 h after the polyunsaturated meal had an inhibitory activity that was greater than that of HDL collected from fasting plasma (p < 0.004 and p = 0.01 for comparison of effect of meals on ICAM-1 and VCAM-1, respectively). Post-hyperemic microvascular flow significantly increased at 3 h after the polyunsaturated meal by 45 +/- 14% and by 21 +/- 11% after the saturated meal. The FMD decreased 3 h after the saturated meal by 2.2 +/- 0.9% (p< 0.05 compared with baseline) and by 0.9 +/- 1% after the polyunsaturated meal.
  
  
  CONCLUSIONS
  Consumption of a saturated fat reduces the anti-inflammatory potential of HDL and impairs arterial endothelial function. In contrast, the anti-inflammatory activity of HDL improves after consumption of polyunsaturated fat. These findings highlight novel mechanisms by which different dietary fatty acids may influence key atherogenic processes.
authors.affiliation: The Heart Research Institute, Sydney, Australia.
authors.forename: Stephen J
authors.initials: SJ
authors.lastname: Nicholls
authors.forename: Pia
authors.initials: P
authors.lastname: Lundman
authors.forename: Jason A
authors.initials: JA
authors.lastname: Harmer
authors.forename: Belinda
authors.initials: B
authors.lastname: Cutri
authors.forename: Kaye A
authors.initials: KA
authors.lastname: Griffiths
authors.forename: Kerry-Anne
authors.initials: KA
authors.lastname: Rye
authors.forename: Philip J
authors.initials: PJ
authors.lastname: Barter
authors.forename: David S
authors.initials: DS
authors.lastname: Celermajer
mesh_terms: D000328:Adult; D015415:Biomarkers / Q000378:metabolism; D008076:Cholesterol, HDL / Q000276:immunology / Q000378:metabolism*; D044842:Cullin Proteins / Q000378:metabolism; D004041:Dietary Fats / Q000009:adverse effects*; D004730:Endothelium, Vascular / Q000378:metabolism; D005260:Female; D006439:Hemodynamics; D006801:Humans; D007249:Inflammation; D018799:Intercellular Adhesion Molecule-1 / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D019518:Postprandial Period; D017483:Receptors, Vasopressin / Q000378:metabolism
chemical_list: D015415:Biomarkers; C496871:CUL5 protein, human; D008076:Cholesterol, HDL; D044842:Cullin Proteins; D004041:Dietary Fats; D017483:Receptors, Vasopressin; D018799:Intercellular Adhesion Molecule-1