title: Effects of C358A missense polymorphism of the endocannabinoid degrading enzyme fatty acid amide hydrolase on weight loss and cardiovascular risk factors 1 year after biliopancreatic diversion surgery.
abstract: BACKGROUND
  Bariatric surgery is the most effective long-term treatment of morbid obesity and also results in a reduction of obesity-associated co-morbidities. We investigated the role of the polymorphism (C358A) of the fatty acid amide hydrolase gene on the clinical outcomes 1 year after biliopancreatic diversion in morbidly obese patients.
  
  
  METHODS
  A total of 67 morbidly obese patients (body mass index >40 kg/m(2)) underwent biliopancreatic diversion. Their weight, blood pressure, basal glucose, triglycerides, total cholesterol, low-density lipoprotein cholesterol, and high-density lipoprotein cholesterol were measured at the baseline visit and at each follow-up visit. The frequency of the metabolic co-morbidities was recorded at each visit.
  
  
  RESULTS
  Of the 67 patients, 46 (68.7%) had genotype C358C (wild-type group) and 21 (10.3%) had genotype C358A (mutant-type group). In the wild- and mutant-type groups, the body mass index, weight, waist circumference, systolic blood pressure, and glucose, total cholesterol, low-density lipoprotein cholesterol, and triglyceride concentrations decreased, without statistical significance between the 2 groups. The initial percentage of weight loss at 9 months and 1 year of follow-up was greater in the mutant-type group (9 months, 22.1% versus 28.8%, P <.05; and 1 year, 28.3% versus 36.4%, P <.05).
  
  
  CONCLUSIONS
  The allele A358 of fatty acid amide hydrolase was associated with a better initial percentage of excess weight loss 9 and 12 months after biliopancreatic diversion.
authors.affiliation: Center of investigation of Endocrinology and Clinical Nutrition, University of Valladolid Medical School and Unit of Investigation, Hospital Rio Hortega, Valladolid, Spain. dadluis@yahoo.es
authors.forename: D A
authors.initials: DA
authors.lastname: de Luis
authors.forename: M Gonzalez
authors.initials: MG
authors.lastname: Sagrado
authors.forename: D
authors.initials: D
authors.lastname: Pacheco
authors.forename: M C
authors.initials: MC
authors.lastname: Terroba
authors.forename: T
authors.initials: T
authors.lastname: Martin
authors.forename: L
authors.initials: L
authors.lastname: Cuellar
authors.forename: M
authors.initials: M
authors.lastname: Ventosa
mesh_terms: D000328:Adult; D000483:Alleles; D000581:Amidohydrolases / Q000235:genetics*; D015904:Biliopancreatic Diversion; D015992:Body Mass Index; D063385:Cannabinoid Receptor Modulators / Q000235:genetics*; D002318:Cardiovascular Diseases / Q000235:genetics*; D015897:Comorbidity; D063388:Endocannabinoids; D005260:Female; D020022:Genetic Predisposition to Disease; D005838:Genotype; D006801:Humans; D008055:Lipids / Q000097:blood; D008297:Male; D009767:Obesity, Morbid / Q000235:genetics* / Q000601:surgery*; D011110:Polymorphism, Genetic; D012307:Risk Factors; D018709:Statistics, Nonparametric; D015431:Weight Loss / Q000235:genetics; D000099252:Fatty Acid Amide Hydrolases
chemical_list: D000581:Amidohydrolases; D063385:Cannabinoid Receptor Modulators; D063388:Endocannabinoids; D008055:Lipids; D000099252:Fatty Acid Amide Hydrolases