title: C358A missense polymorphism of the endocannabinoid-degrading enzyme fatty acid amide hydrolase (FAAH) and visfatin levels in obese females.
abstract: BACKGROUND
  Recently, it has been shown that the polymorphism 385 C/A of FAAH (fatty acid amide hydrolase) was associated with overweight and obesity. Visfatin has been identified as a protein expressed in visceral adipose tissue with contradictory functions in glucose metabolism.
  
  
  OBJECTIVE
  The aim of our study was to investigate the relationship between polymorphism (cDNA 385 C->A) of the FAAH gene and visfatin levels in obese women.
  
  
  METHODS
  A population of 143 females with obesity was analyzed. Indirect calorimetry, tetrapolar electrical bioimpedance, blood pressure and serial assessment of nutritional intake with 3-day written food records and biochemical analysis (lipid profile, visfatin, insulin, C-reactive protein and homeostasis model assessment for insulin sensitivity (HOMA)) were performed.
  
  
  RESULTS
  Ninety-four patients (65.7%) had the genotype C358C (wild-type group) and 49 (34.3%) patients had the genotype C358A (mutant type group). No differences were detected between groups in anthropometric parameters and dietary intakes. Insulin (15.6+/-7.6 vs 14.1+/-10.1 mUI l(-1); P<0.05), glucose (101.2+/-21.9 vs 92.3+/-10.5 mg per 100 ml; P<0.05) and HOMA values (3.96+/-2.3 vs 3.15+/-2.8; P<0.05) were higher in the wild type-group than in the mutant type group. Visfatin levels were lower in the wild-type group than in the mutant type group (47.83+/-57.5 vs 65.71+/-55 ng ml(-1); P<0.05).
  
  
  CONCLUSIONS
  The novel finding of this study is the association of the mutant type group A358C of FAAH with lower glucose, insulin and HOMA levels than of the wild-type group with higher visfatin levels.
authors.affiliation: Institute of Endocrinology and 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: M
authors.initials: M
authors.lastname: Gonzalez 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: D000581:Amidohydrolases / Q000235:genetics*; D001786:Blood Glucose / Q000378:metabolism; D063385:Cannabinoid Receptor Modulators / Q000378:metabolism; D063388:Endocannabinoids; D005260:Female; D005838:Genotype; D006801:Humans; D007328:Insulin / Q000097:blood; D007333:Insulin Resistance; D008875:Middle Aged; D020125:Mutation, Missense / Q000235:genetics*; D054409:Nicotinamide Phosphoribosyltransferase / Q000097:blood*; D009765:Obesity / Q000097:blood / Q000201:enzymology / Q000235:genetics*; D011110:Polymorphism, Genetic / Q000235:genetics; D000099252:Fatty Acid Amide Hydrolases
chemical_list: D000581:Amidohydrolases; D001786:Blood Glucose; D063385:Cannabinoid Receptor Modulators; D063388:Endocannabinoids; D007328:Insulin; D054409:Nicotinamide Phosphoribosyltransferase; D000099252:Fatty Acid Amide Hydrolases