title: Relation of C358A polymorphism of the endocannabinoid degrading enzyme fatty acid amide hydrolase (FAAH) with obesity and insulin resistance.
abstract: OBJECTIVE
  Recently, it has been demonstrated that the polymorphism 385 C->A of FAAH (fatty acid amide hydrolase) was associated with overweight and obesity. The aim of our study was to investigate the relationship of missense polymorphism (cDNA 385 C-A) of FAAH gene on obesity anthropometric parameters, cardiovascular risk factors and adipocytokines.
  
  
  METHODS
  A population of 279 females with obesity (body mass index 30) was analyzed. An indirect calorimetry, tetrapolar electrical bioimpedance, blood pressure, a serial assessment of nutritional intake with 3 days written food records and biochemical analysis (lipid profile, adipocytokines, insulin, CRP and lipoprotein-a) were performed. The statistical analysis was performed for the combined C385A and A385A as a group and wild type C385C as second group.
  
  
  RESULTS
  One hundred and ninety four patients (69.5%) had the genotype C385C (wild type group) and 76 (27.2%) patients had the genotype C358A or A358A (9 patients, 3.2%) (mutant type group). No differences were detected between groups in anthropometric parameters and dietary intakes. Triglycerides (118.9 ± 59.9 mg/dl vs 107.4 + 51.3 mg/dl;p < 0,05), glucose (100.4 ± 19.9 mg/dl vs 94.8 + 11.5mg/dl; p < 0,05), HOMA (3.74 ± 2.2 vs 3.39 + 2.7; p < 0,05) and interleukine 6 (3.3 ± 1.4 pg/ml vs 1.4 ± 2.1 pg/ml; p < 0,05) were higher in wild type group than mutant type group.
  
  
  CONCLUSIONS
  The novel finding of this study is the association of the mutant type group A358C and A358A of FAAH with a better cardiovascular profile (triglyceride, glucose, interleukine 6 and HOMA levels) than wild type group.
authors.affiliation: Center of Investigation of Endocrinology and Clinical Nutrition, Medicine School, 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: González 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
mesh_terms: D054392:Adipokines / Q000097:blood; D000328:Adult; D000581:Amidohydrolases / Q000235:genetics* / Q000378:metabolism*; D000886:Anthropometry; D001786:Blood Glucose / Q000378:metabolism; D002153:Calorimetry, Indirect; D063385:Cannabinoid Receptor Modulators / Q000378:metabolism*; D018076:DNA, Complementary / Q000235:genetics; D063388:Endocannabinoids; D005247:Feeding Behavior; D005260:Female; D005838:Genotype; D006801:Humans; D007333:Insulin Resistance / Q000235:genetics* / Q000502:physiology*; D008055:Lipids / Q000097:blood; D008875:Middle Aged; D020125:Mutation, Missense / Q000502:physiology; D009765:Obesity / Q000201:enzymology* / Q000235:genetics*; D011110:Polymorphism, Genetic; D011446:Prospective Studies; D012307:Risk Factors; D000099252:Fatty Acid Amide Hydrolases
chemical_list: D054392:Adipokines; D000581:Amidohydrolases; D001786:Blood Glucose; D063385:Cannabinoid Receptor Modulators; D018076:DNA, Complementary; D063388:Endocannabinoids; D008055:Lipids; D000099252:Fatty Acid Amide Hydrolases