title: Relationship among metabolic syndrome, C358A polymorphism of the endocannabinoid degrading enzyme fatty acid amide hydrolase (FAAH) and insulin resistance.
abstract: BACKGROUND
  It has been demonstrated that the polymorphism 385 C/A of FAAH (fatty acid amide hydrolase) was associated with obesity and metabolic disorders.
  
  
  OBJECTIVE
  The aim of our study was to investigate the relationship of the polymorphism (cDNA 385 C->A) of FAAH gene and insulin resistance in obese patients with and without metabolic syndrome.
  
  
  METHODS
  A population of 799 obese patients was analyzed in cross-sectional survey. A bioimpedance, blood pressure, serial assessment of nutritional intake with 3 days written food records and biochemical analysis were performed. Genotype of FAAH gene polymorphism was studied.
  
  
  RESULTS
  Prevalence of metabolic syndrome (MS) with ATP III definition was 49.8% (398 patients) and 50.2% patients without MS (n=401 patients). Prevalence of FAAH genotypes was similar in patients with metabolic syndrome (69.6% wild genotype and 30.4% mutant genotype) and without metabolic syndrome (66.6% wild genotype and 33.4% mutant genotype). In patients without metabolic syndrome, insulin and HOMA levels were higher in mutant genotype than wild type group.
  
  
  CONCLUSIONS
  The main finding is the lack of association of the FAAH genotypes with metabolic syndrome prevalence. Patients with mutant genotype group of FAAH gene and without metabolic syndrome have higher insulin and HOMA levels than wild type group.
authors.affiliation: Center of Investigation of Endocrinology and Clinical Nutrition, Medicine School and Unit of Investigation, Hospital Rio Hortega, University of Valladolid, Valladolid, Spain. dadluis@yahoo.es
authors.forename: D A
authors.initials: DA
authors.lastname: de Luis
authors.forename: R
authors.initials: R
authors.lastname: Aller
authors.forename: O
authors.initials: O
authors.lastname: Izaola
authors.forename: R
authors.initials: R
authors.lastname: Conde
authors.forename: M Gonzalez
authors.initials: MG
authors.lastname: Sagrado
authors.forename: D
authors.initials: D
authors.lastname: Primo
authors.forename: M J
authors.initials: MJ
authors.lastname: Castro
mesh_terms: D000328:Adult; D000581:Amidohydrolases / Q000235:genetics*; D015897:Comorbidity; D003430:Cross-Sectional Studies; D005260:Female; D005838:Genotype; D006706:Homeostasis; D006801:Humans; D007328:Insulin / Q000097:blood; D007333:Insulin Resistance / Q000235:genetics*; D008297:Male; D024821:Metabolic Syndrome / Q000097:blood / Q000453:epidemiology* / Q000235:genetics*; D008875:Middle Aged; D009765:Obesity / Q000097:blood / Q000453:epidemiology* / Q000235:genetics*; D011110:Polymorphism, Genetic / Q000235:genetics*; D015995:Prevalence; D000099252:Fatty Acid Amide Hydrolases
chemical_list: D000581:Amidohydrolases; D007328:Insulin; D000099252:Fatty Acid Amide Hydrolases