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Friday, January 20, 2017

Primary TMAU and Secondary TMAU

On this 2016 paper previous mentioned on a post in this blog, 'New Phillips/Shephard TMAU & FMO3 overview paper', the authors give us the definition of Primary TMAU and Secondary TMAU.


"Trimethylamine and Trimethylamine N-Oxide, a Flavin-Containing Monooxygenase 3 (FMO3)-Mediated Host-Microbiome Metabolic Axis Implicated in Health and Disease"
Published in ASPET, DRUG METABOLISM AND DISPOSITION
Diede Fennema, Ian R. Phillips and Elizabeth A. Shephard
Drug Metabolism and Disposition November 2016, 44 (11) 1839-1850; DOI: https://doi.org/10.1124/dmd.116.070615

TMAU, a Deficiency of FMO3


Primary Trimethylaminuria:


In humans, mutations that abolish or severely impair the activity of FMO3 cause the inherited disorder primary TMAU (Dolphin et al., 1997Hernandez et al., 2003). Affected individuals have a severely reduced ability to convert TMA to TMAO and, consequently, excrete large amounts of odorous TMA in their urine, sweat, and breath (Ayesh et al., 1993). Although the disorder has no overt physiologic effects on patient health, it can have profound psychologic and social consequences, resulting in a severe loss of quality of life, in extreme cases giving rise to clinical depression and suicidal tendencies (Mitchell and Smith, 2001Shephard et al., 2015, [Phillips IR and Shephard EA. Primary trimethylaminuria. GeneReviews at GeneTests: Medical Genetics Information Resource (database online): University of Washington, 1997––2015 available at http://www.ncbi.nlm.nih.gov/books/NBK1103/, updated 2015]. In terms of drug metabolism, TMAU individuals have impaired metabolism of the FMO3 drug substrate benzydamine (Mayatepek et al., 2004). Since the first discovery of a mutation known to cause TMAU (Dolphin et al., 1997), many different causative mutations have been identified (Phillips et al., 2007Yamazaki and Shimizu, 2013). A catalog of variants of the FMO3 gene and their effect on the ability of FMO3 to catalyze the oxygenation of TMA and drug substrates of the enzyme can be accessed at the FMO3 locus-specific mutation database (http://databases.lovd.nl/shared/genes/FMO3).

Secondary Trimethylaminuria:


Production of large amounts of TMA, as a result of gut microbial action, exacerbates the symptoms of primary TMAU. In addition, overproduction of TMA, as a consequence of a dysbiosis of the gut microbiome, can give rise to a nongenetic form of the disorder, known as secondary TMAU (Mitchell and Smith, 2001). Therefore, a better understanding of the bacterial species that produce TMA in the gut may provide insights into why some individuals develop secondary TMAU in the absence of impaired N-oxygenation of TMA (Shimizu et al., 2014) and offers the potential to develop improved strategies for the management and treatment of both primary and secondary forms of the disorder.

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