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Fatty acid amide hydrolase 2 degrades many types of fatty acid amides, including the sleep-inducing oleamide and endocannabinoids such as anandamide.[4] It has a tissue distribution quite distinct from the paralogous FAAH (or "FAAH1"). Compared to FAAH, it is less active on N-acyl ethanolamines (e.g. anandamide) and N-acyl taurines.[3]
OrthoDB indicates that FAAH2 (as a gene distinct from FAAH) has orthologs all across Metazoa, with the notable exclusion of rodents.[5] This complicates the translation of FAAH-related results from rodent models to human biology.[3]
Defects in this enzyme have been associated with neurologic and psychiatric disorders. Specifically, a Canadian male with autism, anxiety, severe dysarthria, and a number of other issues have a Ala458Ser mutation inherited from his healthy carrier mother. In cell models this mutation is associated with a decreased function of this gene. This patient has a very abnormal blood lipid composition consistent with a loss of function.[6]
ClinVar reports a missense mutation that produces an early stop codon (Trp392Ter) is associated with Meckel-like syndrome.[7]
UniProt Variant Viewer lists a large number of other variants found in surveyed human genomes. Several are predicted to have consequences by PolyPhen and/or SIFT.[4]
