C358A missense polymorphism of the endocannabinoid-degrading enzyme fatty acid amide hydrolase (FAAH) and visfatin levels in obese females.

Abstract

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. 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. 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. 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). 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.