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Fish Odor Syndrome/Trimethylaminuria
Published in Charles Theisler, Adjuvant Medical Care, 2023
Diet: Affected individuals must lower intake of chemical precursors to trimethylamine such as choline, lecithin, and carnitine (e.g., saltwater fish, liver, kidneys, eggs, peas, and soybeans) consumption.1
The Role of the Gut Microbiome in Cardiovascular Disease
Published in Stephen T. Sinatra, Mark C. Houston, Nutritional and Integrative Strategies in Cardiovascular Medicine, 2022
The gut microbiota is an important player in atherogenesis.14 Specifically, higher levels of Lactobacillales and decreased levels in Bacteroides have been associated with coronary artery disease.15 Metabolism by certain intestinal flora has been linked to the deleterious association between the development of atherosclerotic plaque and egg yolk consumption, due to its choline content. Certain gut microbiota can metabolize choline, phosphatidylcholine,16 and L-carnitine17 to produce trimethylamine (TMA), which can be oxidized in the liver into trimethylamine N-oxide (TMAO), a proatherogenic metabolite. Inhibiting TMAO production through the gut microbiota has been found to be a promising treatment for atherosclerosis.18 Due to the inherent complexity of the gut microbiome and its differences among individuals, this pathway is not the same for everyone. The complex ecology of the gut microbiota and its role in metabolic behavior must be considered. For example, many types of fish are still considered beneficial for cardiovascular patients19 despite their trimethylamine content. Additionally, L-carnitine may ameliorate metabolic diseases20 by increasing insulin sensitivity of the skeletal muscle and may reduce ischemic heart disease in some people.
Future Developments of Multinuclear NMR Spectroscopy (MRS) in Clinical Examinations
Published in Bertil R. R. Persson, Freddy Ståhlberg, Health and Safety of Clinical NMR Examinations, 2019
Bertil R. R. Persson, Freddy Ståhlberg
A problem that may limit the usefulness of 14N-NMR in intact tissue is the rapid exchange of nitrogen compounds in solution with those bound to sites on macromolecules. Such interactions tend to broaden the 14N resonance signal considerably. The binding of urea to intra- and extracellular proteins is presented by Balaban and Knepper3 as a specific example of this phenomenon. A particularly interesting finding was the high concentration («90 mM) of trimethylamine compounds in the renal inner medulla. Balaban and Knepper3 proposed that 14N-NMR is a potentially useful technique for noninvasive detection of specific nitrogen-containing compounds in intact biological tissue.
Flavin-containing monooxygenase 3 (FMO3): genetic variants and their consequences for drug metabolism and disease
Published in Xenobiotica, 2020
Ian R. Phillips, Elizabeth A. Shephard
A major impetus for investigating FMOs of human was to identify the molecular basis of the recessively inherited disorder trimethylaminuria (OMIM 602079) and build on the earlier work of Bob Smith and colleagues in characterizing the disorder and establishing its mode of inheritance (Al-Waiz et al., 1987; reviewed in Mitchell & Smith, 2001). The disorder is characterized by the excretion of excessive amounts of the smelly tertiary amine trimethylamine in urine, sweat, breath and reproductive fluids, which imparts an odour characteristic of rotten fish (Mitchell & Smith, 2001, 2003). The trimethylamine is derived from dietary precursors, via the action of gut bacteria (reviewed in Fennema et al., 2016). Affected individuals are defective in the hepatic metabolism of trimethylamine to its non-odorous N-oxide (reviewed in Mitchell & Smith, 2001; Phillips & Shephard, 2015; Shephard et al., 2015), a reaction that is selectively catalyzed by FMO3 (Lang et al., 1998). Although no overt physical symptoms are associated with trimethylaminuria, the unpleasant odour characteristic of the disorder often results in psychological and social problems, including anxiety, chronic depression and, in extreme cases, suicidal tendencies (Mitchell & Smith, 2001).
Novel variants and haplotypes of human flavin-containing monooxygenase 3 gene associated with Japanese subjects suffering from trimethylaminuria
Published in Xenobiotica, 2019
Makiko Shimizu, Hiromi Yoda, Narumi Igarashi, Miki Makino, Emi Tokuyama, Hiroshi Yamazaki
Humans livers contain functional form 3 of flavin-containing monooxygenase (FMO; EC 1.14.13.8), designated FMO3. FMO3 catalyzes NADPH-dependent oxidations of a wide range of xenobiotics that include dietary components, environmental chemicals, and therapeutic drugs (Fennema et al., 2016; Krueger & Williams, 2005; Phillips & Shephard, 2017). Food-derived choline and carnitine are often metabolized by the intestinal microbiota to trimethylamine, which is absorbed by the gut. This trimethylamine is then further oxidized to trimethylamine N-oxide by FMO3 in the liver (Collins et al., 2016). The levels of trimethylamine and its N-oxide resulting from daily dietary consumption (Fennema et al., 2016) and prescribed l-carnitine (Bain et al., 2006) are accepted as nontoxic (WHO, 2006). The no-observable-adverse-effect level of trimethylamine for general toxicity was estimated to be 160 mg/kg/day in rats, implying little risk in humans from normal daily dietary intake (Amoore et al., 1978). Despite previous research having established the safety of trimethylamine and its N-oxide, clinical interest in the safety of these compounds has recently arisen because circulating trimethylamine N-oxide levels in plasma have been associated with atherosclerotic heart disease. (Bennett et al., 2013). Individuals harboring defective FMO3 alleles may suffer from trimethylaminuria (OMIM No. 602079), a disorder in which excessive amounts of trimethylamine are excreted in bodily secretions including urine, sweat and reproductive fluids (Allerston et al., 2009; Shephard et al., 2012, 2015). Consequently, people who have trimethylaminuria exhibit an unpleasant body and breath odor and suffer the social and psychological problems associated with body malodours (Mitchell & Smith, 2001).