title: High-density lipoprotein subfractions display proatherogenic properties in overweight and obese children.
abstract: BACKGROUND
  In adults, obesity-driven inflammation can lead to increased cardiovascular disease (CVD). However, information regarding childhood obesity and its inflammatory sequelae is less well defined. Serum amyloid-A (SAA) is an inflammatory molecule that rapidly associates with high-density lipoproteins (HDLs) and renders them dysfunctional. Therefore, SAA may be a useful biomarker to identify increased CVD potential in overweight and obese children.
  
  
  METHODS
  Young Hearts 2000 is a cross-sectional cohort study in which 92 children who were obese were matched for age and sex with 92 overweight and 92 lean children. HDL(2) and HDL(3) (HDL(2&3)) were isolated from plasma by a three-step rapid-ultracentrifugation procedure. SAA was measured in serum and HDL(2&3) by an enzyme-linked immunosorbent assay procedure, and the activities of cholesterol ester transfer protein (CETP) and lecithin cholesteryl acyltransferase (LCAT) were measured by fluorimetric assays.
  
  
  RESULTS
  Trends across the groups indicated that SAA increased in serum and HDL(2&3) as BMI increased, as did HDL(2)-CETP and HDL(2)-LCAT activities.
  
  
  CONCLUSIONS
  These results have provided evidence that overweight and obese children are exposed to an inflammatory milieu that impacts the antiatherogenic properties of HDL and that could increase CVD risk. This supports the concept that it is important to target childhood obesity to help minimize future cardiovascular events.
authors.affiliation: Centre for Public Health, Nutrition and Metabolism Group, Queen's University Belfast, Belfast, UK. j.mceneny@qub.ac.uk
authors.forename: Jane
authors.initials: J
authors.lastname: McEneny
authors.forename: Sarah
authors.initials: S
authors.lastname: Blair
authors.forename: Jayne V
authors.initials: JV
authors.lastname: Woodside
authors.forename: Liam
authors.initials: L
authors.lastname: Murray
authors.forename: Colin
authors.initials: C
authors.lastname: Boreham
authors.forename: Ian S
authors.initials: IS
authors.lastname: Young
mesh_terms: D000293:Adolescent; D000704:Analysis of Variance; D050197:Atherosclerosis / Q000209:etiology*; D002097:C-Reactive Protein / Q000032:analysis; D002648:Child; D053480:Cholesterol Ester Transfer Proteins / Q000097:blood; D015331:Cohort Studies; D003430:Cross-Sectional Studies; D006801:Humans; D053439:Lipoproteins, HDL2 / Q000097:blood*; D053440:Lipoproteins, HDL3 / Q000097:blood*; D009391:Nephelometry and Turbidimetry; D009765:Obesity / Q000097:blood / Q000150:complications*; D050177:Overweight / Q000097:blood / Q000150:complications*; D007862:Phosphatidylcholine-Sterol O-Acyltransferase / Q000097:blood; D000685:Serum Amyloid A Protein / Q000032:analysis; D014461:Ultracentrifugation
chemical_list: C506642:CETP protein, human; D053480:Cholesterol Ester Transfer Proteins; D053439:Lipoproteins, HDL2; D053440:Lipoproteins, HDL3; D000685:Serum Amyloid A Protein; D002097:C-Reactive Protein; D007862:Phosphatidylcholine-Sterol O-Acyltransferase