ArticleBMC medical genetics2010
Mutation screen and association studies for the fatty acid amide hydrolase (FAAH) gene and early onset and adult obesity.
Article in BMC medical genetics, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled it.
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Who cites it
8 citing papers in PubMed, 1 synthesis or guideline pooled it, 24 citations in OpenAlex.
- Association between the FAAH C385A variant (rs324420) and obesity-related traits: a systematic review.International journal of obesity (2005) · 2024Pooled it
- Sweet Taste Receptors' Genetic Variability in Advanced Potential Targets of Obesity.Nutrients · 2025Article
- Interplays of Dietary Fat with BMI andFood science & nutrition · 2024Article
- Review
- Potential of Fatty Acid Amide Hydrolase (FAAH), Monoacylglycerol Lipase (MAGL), and Diacylglycerol Lipase (DAGL) Enzymes as Targets for Obesity Treatment: A Narrative Review.Pharmaceuticals (Basel, Switzerland) · 2021Review
- Review
- The hepatic cannabinoid 1 receptor as a modulator of hepatic energy state and food intake.British journal of clinical pharmacology · 2014Review
- 385 C/A polymorphism of the fatty acid amide hydrolase gene is associated with metabolic syndrome in the Chinese Han population.Archives of medical science : AMS · 2011Article
Corrections and comments
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Authors and funding
16 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe orexigenic effects of cannabinoids are limited by activation of the endocannabinoid degrading enzyme fatty acid amide hydrolase (FAAH). The aim of this study was to analyse whether FAAH alleles are associated with early and late onset obesity.
methodsWe initially assessed association of five single nucleotide polymorphisms (SNPs) in FAAH with early onset extreme obesity in up to 521 German obese children and both parents. SNPs with nominal p-values <or= 0.1 were subsequently analysed in 235 independent German obesity families. SNPs associated with childhood obesity (p-values <or2= 0.05) were further analysed in 8,491 adult individuals of a population-based cohort (KORA) for association with adult obesity. One SNP was further analysed in 985 German obese adults and 588 normal and underweight controls. In parallel, we screened the FAAH coding region for novel sequence variants in 92 extremely obese children using single-stranded-conformation-polymorphism-analysis and denaturing HPLC and assessed the implication of the identified new variants for childhood obesity.
resultsThe trio analysis revealed some evidence for an association of three SNPs in FAAH (rs324420 rs324419 and rs873978) with childhood obesity (two-sided p-values between 0.06 and 0.10). Although analyses of these variants in 235 independent obesity families did not result in statistically significant effects (two-sided p-values between 0.14 and 0.75), the combined analysis of all 603 obesity families supported the idea of an association of two SNPs in FAAH (rs324420 and rs2295632) with early onset extreme obesity (p-values between 0.02 and 0.03). No association was, however, found between these variants and adult obesity. The mutation screen revealed four novel variants, which were not associated with early onset obesity (p > 0.05).
conclusionsAs we observed some evidence for an association of the FAAH variants rs2295632 rs324420 with early onset but not adult obesity, we conclude that the FAAH variants analyzed here at least do not seem to play a major role in the etiology of obesity within our samples.
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