title: C358A missense polymorphism of the endocannabinoid degrading enzyme fatty acid amide hydrolase (FAAH) and insulin resistance in patients with diabetes mellitus type 2.
abstract: BACKGROUND
  The polymorphism 385 C/A of FAAH has been associated with overweight and obesity. The aim of our study was to investigate the relationship of polymorphism (cDNA 385 C-->A) of FAAH gene on obesity parameters in patients with diabetes mellitus type 2.
  
  
  METHODS
  A population of 70 patients with diabetes mellitus type 2 was analyzed. An anthropometric and biochemical nutritional assessment was performed. The statistical analysis was performed for the combined C358A and A358A as a group and wild type C358C as second group.
  
  
  RESULTS
  Fifty-five patients (78.7%) had genotype C358C (wild type group) and 15 (21.3%) patients C358A (14 patients, 20.6%) or A358A (1 patient, 0.7%) (mutant group). BMI (38.9+/-6.4 vs. 39.2+/-5.7, p<0.05), weight (96.8+/-17.6kg vs. 102.5+/-16.8kg, p<0.05), fat mass (42.1+/-16.1kg. vs. 46.9+/-11.1kg, p<0.05), waist circumference (115.9+/-12.8cm vs. 121.3+/-12.8cm, p<0.05), insulin (22.5+/-18.8mUI/L vs. 33.9+/-17.1UI/L, p<0.05) and TNF-alpha (6.1+/-3.4pg/mL vs. 8.4+/-3.2pg/mL, p<0.05) were higher in mutant type group than wild type. Adiponectin levels (33.3+/-20.8ng/mL vs. 22.3+/-10.8ng/mL, p<0.05) were higher in wild type group than mutant type group.
  
  
  CONCLUSIONS
  There is an association of the mutant type group A358C and A358A of FAAH with a worse cardiovascular profile (weight, body mass index, waist circumference, insulin,TNF-alpha and adiponectin levels) than wild type group.
authors.affiliation: Institute of Endocrinology and Nutrition, Medicine School and Unit of Investigation, Hospital Rio Hortega, University of Valladolid, C/Los perales 16, Simancas 47130, RETICEF RD056/0013, 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: 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: E
authors.initials: E
authors.lastname: Romero
mesh_terms: D052242:Adiponectin / Q000097:blood; D000328:Adult; D000368:Aged; D000581:Amidohydrolases / Q000235:genetics*; D001786:Blood Glucose / Q000235:genetics; D001823:Body Composition; D015992:Body Mass Index; D002151:Calorimetry; D002784:Cholesterol / Q000097:blood; D003924:Diabetes Mellitus, Type 2 / Q000097:blood / Q000235:genetics*; D004032:Diet; D004797:Enzyme-Linked Immunosorbent Assay; D005247:Feeding Behavior; D005260:Female; D020022:Genetic Predisposition to Disease; D006801:Humans; D007333:Insulin Resistance / Q000235:genetics*; D008297:Male; D008875:Middle Aged; D020125:Mutation, Missense / Q000235:genetics*; D011110:Polymorphism, Genetic; D052243:Resistin / Q000097:blood; D018709:Statistics, Nonparametric; D014280:Triglycerides / Q000097:blood; D014409:Tumor Necrosis Factor-alpha / Q000097:blood; D000099252:Fatty Acid Amide Hydrolases
chemical_list: D052242:Adiponectin; D000581:Amidohydrolases; D001786:Blood Glucose; D002784:Cholesterol; D052243:Resistin; D014280:Triglycerides; D014409:Tumor Necrosis Factor-alpha; D000099252:Fatty Acid Amide Hydrolases