Relationship among metabolic syndrome, C358A polymorphism of the endocannabinoid degrading enzyme fatty acid amide hydrolase (FAAH) and insulin resistance

J Diabetes Complications. 2012 Jul-Aug;26(4):328-32. doi: 10.1016/j.jdiacomp.2012.04.002. Epub 2012 May 17.

Abstract

Background: It has been demonstrated that the polymorphism 385 C/A of FAAH (fatty acid amide hydrolase) was associated with obesity and metabolic disorders.

Objective: The aim of our study was to investigate the relationship of the polymorphism (cDNA 385 C->A) of FAAH gene and insulin resistance in obese patients with and without metabolic syndrome.

Design: A population of 799 obese patients was analyzed in cross-sectional survey. A bioimpedance, blood pressure, serial assessment of nutritional intake with 3 days written food records and biochemical analysis were performed. Genotype of FAAH gene polymorphism was studied.

Results: Prevalence of metabolic syndrome (MS) with ATP III definition was 49.8% (398 patients) and 50.2% patients without MS (n=401 patients). Prevalence of FAAH genotypes was similar in patients with metabolic syndrome (69.6% wild genotype and 30.4% mutant genotype) and without metabolic syndrome (66.6% wild genotype and 33.4% mutant genotype). In patients without metabolic syndrome, insulin and HOMA levels were higher in mutant genotype than wild type group.

Conclusion: The main finding is the lack of association of the FAAH genotypes with metabolic syndrome prevalence. Patients with mutant genotype group of FAAH gene and without metabolic syndrome have higher insulin and HOMA levels than wild type group.

Publication types

  • Comparative Study

MeSH terms

  • Adult
  • Amidohydrolases / genetics*
  • Comorbidity
  • Cross-Sectional Studies
  • Female
  • Genotype
  • Homeostasis
  • Humans
  • Insulin / blood
  • Insulin Resistance / genetics*
  • Male
  • Metabolic Syndrome / blood
  • Metabolic Syndrome / epidemiology*
  • Metabolic Syndrome / genetics*
  • Middle Aged
  • Obesity / blood
  • Obesity / epidemiology*
  • Obesity / genetics*
  • Polymorphism, Genetic / genetics*
  • Prevalence

Substances

  • Insulin
  • Amidohydrolases
  • fatty-acid amide hydrolase