title: Obesity and body fat classification in the metabolic syndrome: impact on cardiometabolic risk metabotype.
abstract: OBJECTIVE
  Obesity is a key factor in the development of the metabolic syndrome (MetS), which is associated with increased cardiometabolic risk. We investigated whether obesity classification by BMI and body fat percentage (BF%) influences cardiometabolic profile and dietary responsiveness in 486 MetS subjects (LIPGENE dietary intervention study).
  
  
  METHODS
  Anthropometric measures, markers of inflammation and glucose metabolism, lipid profiles, adhesion molecules, and hemostatic factors were determined at baseline and after 12 weeks of four dietary interventions (high saturated fat (SFA), high monounsaturated fat (MUFA), and two low fat high complex carbohydrate (LFHCC) diets, one supplemented with long chain n-3 polyunsaturated fatty acids (LC n-3 PUFAs)).
  
  
  RESULTS
  About 39 and 87% of subjects classified as normal and overweight by BMI were obese according to their BF%. Individuals classified as obese by BMI (≥ 30 kg/m(2)) and BF% (≥ 25% (men) and ≥ 35% (women)) (OO, n = 284) had larger waist and hip measurements, higher BMI and were heavier (P < 0.001) than those classified as nonobese by BMI but obese by BF% (NOO, n = 92). OO individuals displayed a more proinflammatory (higher C reactive protein (CRP) and leptin), prothrombotic (higher plasminogen activator inhibitor-1 (PAI-1)), proatherogenic (higher leptin/adiponectin ratio) and more insulin resistant (higher HOMA-IR) metabolic profile relative to the NOO group (P < 0.001). Interestingly, tumor necrosis factor-α (TNF-α) concentrations were lower post-intervention in NOO individuals compared with OO subjects (P < 0.001).
  
  
  CONCLUSIONS
  In conclusion, assessing BF% and BMI as part of a metabotype may help to identify individuals at greater cardiometabolic risk than BMI alone.
authors.affiliation: Nutrigenomics Research Group, UCD School of Public Health and Population Science, UCD Conway Institute, University College Dublin, Dublin, Ireland.
authors.forename: Catherine M
authors.initials: CM
authors.lastname: Phillips
authors.forename: Audrey C
authors.initials: AC
authors.lastname: Tierney
authors.forename: Pablo
authors.initials: P
authors.lastname: Perez-Martinez
authors.forename: Catherine
authors.initials: C
authors.lastname: Defoort
authors.forename: Ellen E
authors.initials: EE
authors.lastname: Blaak
authors.forename: Ingrid M F
authors.initials: IM
authors.lastname: Gjelstad
authors.forename: Jose
authors.initials: J
authors.lastname: Lopez-Miranda
authors.forename: Malgorzata
authors.initials: M
authors.lastname: Kiec-Klimczak
authors.forename: Malgorzata
authors.initials: M
authors.lastname: Malczewska-Malec
authors.forename: Christian A
authors.initials: CA
authors.lastname: Drevon
authors.forename: Wendy
authors.initials: W
authors.lastname: Hall
authors.forename: Julie A
authors.initials: JA
authors.lastname: Lovegrove
authors.forename: Brita
authors.initials: B
authors.lastname: Karlstrom
authors.forename: Ulf
authors.initials: U
authors.lastname: Risérus
authors.forename: Helen M
authors.initials: HM
authors.lastname: Roche
mesh_terms: D052242:Adiponectin / Q000097:blood; D000273:Adipose Tissue; D001823:Body Composition; D015992:Body Mass Index; D002097:C-Reactive Protein / Q000378:metabolism; D002318:Cardiovascular Diseases / Q000097:blood / Q000209:etiology; D004035:Diet Therapy; D005260:Female; D006801:Humans; D007333:Insulin Resistance; D020738:Leptin / Q000097:blood; D008297:Male; D024821:Metabolic Syndrome / Q000097:blood / Q000150:complications; D008875:Middle Aged; D009765:Obesity / Q000097:blood / Q000150:complications / Q000175:diagnosis; D050177:Overweight; D017395:Plasminogen Activator Inhibitor 1 / Q000097:blood; D012016:Reference Values; D012307:Risk Factors; D014409:Tumor Necrosis Factor-alpha / Q000097:blood
chemical_list: D052242:Adiponectin; D020738:Leptin; D017395:Plasminogen Activator Inhibitor 1; D014409:Tumor Necrosis Factor-alpha; D002097:C-Reactive Protein