title: PPARγ Pro12Ala and ACE ID polymorphisms are associated with BMI and fat distribution, but not metabolic syndrome.
abstract: BACKGROUND
  Metabolic Syndrome (MetS) results from the combined effect of environmental and genetic factors. We investigated the possible association of peroxisome proliferator-activated receptor-γ2 (PPARγ2) Pro12Ala and Angiotensin Converting Enzyme (ACE) I/D polymorphisms with MetS and interaction between these genetic variants.
  
  
  METHODS
  Three hundred sixty four unrelated Caucasian subjects were enrolled. Waist circumference, blood pressure, and body mass index (BMI) were recorded. Body composition was estimated by impedance analysis; MetS was diagnosed by the NCEP-ATPIII criteria. A fasting blood sample was obtained for glucose, insulin, lipid profile determination, and DNA isolation for genotyping.
  
  
  RESULTS
  The prevalence of MetS did not differ across PPARγ2 or ACE polymorphisms. Carriers of PPARγ2 Ala allele had higher BMI and fat-mass but lower systolic blood pressure compared with Pro/Pro homozygotes. A significant PPARγ2 gene-gender interaction was observed in the modulation of BMI, fat mass, and blood pressure, with significant associations found in women only. A PPARγ2-ACE risk genotype combination for BMI and fat mass was found, with ACE DD/PPARγ2 Ala subjects having a higher BMI (p = 0.002) and Fat Mass (p = 0.002). Pro12Ala was independently associated with waist circumference independent of BMI and gender.
  
  
  CONCLUSIONS
  Carriers of PPARγ2 Ala allele had higher BMI and fat-mass but not a worse metabolic profile, possibly because of a more favorable adipose tissue distribution. A gene interaction exists between Pro12Ala and ACE I/D on BMI and fat mass. Further studies are needed to assess the contribution of Pro12Ala polymorphism in adiposity distribution.
authors.affiliation: Department of Clinical and Experimental Medicine, Section of Internal Medicine, Gerontology and Clinical Nutrition, University of Ferrara, Ferrara, Italy. psn@unife.it
authors.forename: Angela
authors.initials: A
authors.lastname: Passaro
authors.forename: Edoardo
authors.initials: E
authors.lastname: Dalla Nora
authors.forename: Caterina
authors.initials: C
authors.lastname: Marcello
authors.forename: Francesca
authors.initials: F
authors.lastname: Di Vece
authors.forename: Mario Luca
authors.initials: ML
authors.lastname: Morieri
authors.forename: Juana M
authors.initials: JM
authors.lastname: Sanz
authors.forename: Cristina
authors.initials: C
authors.lastname: Bosi
authors.forename: Renato
authors.initials: R
authors.lastname: Fellin
authors.forename: Giovanni
authors.initials: G
authors.lastname: Zuliani
mesh_terms: D000328:Adult; D000368:Aged; D019943:Amino Acid Substitution; D001483:Base Sequence; D050218:Body Fat Distribution; D015992:Body Mass Index; D015331:Cohort Studies; D017931:DNA Primers / Q000235:genetics; D005260:Female; D056726:Genetic Association Studies; D006801:Humans; D054643:INDEL Mutation; D008297:Male; D024821:Metabolic Syndrome / Q000209:etiology / Q000235:genetics* / Q000473:pathology; D008875:Middle Aged; D047495:PPAR gamma / Q000235:genetics*; D007703:Peptidyl-Dipeptidase A / Q000235:genetics*; D020641:Polymorphism, Single Nucleotide
chemical_list: D017931:DNA Primers; D047495:PPAR gamma; D007703:Peptidyl-Dipeptidase A