The metabolism of choline by the germfree rat

Prentiss, Phoebe G.; Rosen, Harvey M.; Brown, Nesbitt D.; Horowitz, Richard E.; Malm, Ole J.; Levenson, Stanley Μ.

doi:10.1016/0003-9861(61)90069-8

Cited by 36 publications

(15 citation statements)

References 9 publications

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“…The study by Zhang et al has revealed that there may be increased formation of TMA when the pure chemical form of these precursors is administered to humans as compared to the ingestion as a component of whole food [6]. Studies have also confirmed that choline and L-carnitine undergo carrier mediated absorption [57][58][59][60][61][62][63], meaning that the administration of higher oral doses of these precursors would result in increased generation of TMA [10]. However, Gas chromatography (solid-phase microextraction) Urine Aqueous 0.8 µM to 157 µM Mills et al [39] Gas chromatography (derivitization with 2,2,2-trichloroethylchloroformate) Urine Blood 1pmol to 250 pmol Da Costa et al [41] Fast atom bombardment-mass spectrometry Urine 7 µM to 135 µM Mamer et al [46] Proton nuclear magnetic resonance spectroscopy Urine Abeling et al [44] HPLC (conductimetric detection) Urine Marzo et al [43] HPLC (refractive index) Urine Marzo et al [43] differences in gastrointestinal physiology between animals and humans [64] (for instance the human small intestine is reported to have a lower absorptive capacity for L-carnitine than the rat [52]) could mean that the fate of these chemical precursors may also be dissimilar.…”

Section: Dietary Precursorsmentioning

confidence: 89%

“…However, Gas chromatography (solid-phase microextraction) Urine Aqueous 0.8 µM to 157 µM Mills et al [39] Gas chromatography (derivitization with 2,2,2-trichloroethylchloroformate) Urine Blood 1pmol to 250 pmol Da Costa et al [41] Fast atom bombardment-mass spectrometry Urine 7 µM to 135 µM Mamer et al [46] Proton nuclear magnetic resonance spectroscopy Urine Abeling et al [44] HPLC (conductimetric detection) Urine Marzo et al [43] HPLC (refractive index) Urine Marzo et al [43] differences in gastrointestinal physiology between animals and humans [64] (for instance the human small intestine is reported to have a lower absorptive capacity for L-carnitine than the rat [52]) could mean that the fate of these chemical precursors may also be dissimilar. Enterobacteria are involved in the degradation of dietary components such as choline into TMA [9][10][11][12][13][14]. Evidence for this degradation has emerged from studies conducted in animals where there is a decrease in the urinary excretion of TMA in germ free animals as compared to the normal controls [10,12,65].…”

Section: Dietary Precursorsmentioning

confidence: 99%

“…Following the ingestion of food containing precursors to TMA, such as choline found in egg yolk, enterobacteria are involved in the generation of TMA [9][10][11][12][13][14]. The physicochemical properties of TMA permit efficient absorption from the gastrointestinal tract [15] with subsequent extensive Noxidation by the human liver to form the odorless TMNO [16,17]; the flavin-containing monooxygenase (FMO) enzyme (EC 1.14.13.8) isoform 3 is involved in the conversion of TMA to TMNO [17,18].…”

Section: Introductionmentioning

confidence: 99%

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Trimethylamine: Metabolic, Pharmacokinetic and Safety Aspects

Bain¹,

Fornasini²,

Evans

2005

CDM

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Trimethylamine (TMA) is a volatile tertiary aliphatic amine that is derived from the diet either directly from the consumption of foods containing TMA, or by the intake of food containing precursors to TMA such as trimethylamine-N-oxide (TMNO), choline and L-carnitine. Following oral absorption in humans, TMA undergoes efficient N-oxidation to TMNO, a reaction catalyzed by the flavin-containing monooxygenase (FMO) isoform 3 enzyme. TMNO subsequently undergoes excretion in the urine, although, evidence also suggests that metabolic retro-reduction of TMNO can occur. Whilst the pharmacokinetics of TMA and TMNO has not been fully elucidated in humans, a number of studies provide information on the likely fate of dietary derived TMA. Trimethylaminuria is a condition that is characterized by a deficiency in FMO3 enzyme activity, resulting in the excretion of increased amounts of TMA in bodily fluids such as urine and sweat, and breath. A human FMO3 database has been established and currently twenty-eight variants of the FMO3 gene have been reported including twenty-four missense, three nonsense, and one gross deletion mutation. Whilst TMA and TMNO are generally regarded as non-toxic substances, they are of clinical interest because of their potential to form the carcinogen N-nitrosodimethylamine.

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Section: Dietary Precursorsmentioning

confidence: 89%

Section: Dietary Precursorsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Trimethylamine: Metabolic, Pharmacokinetic and Safety Aspects

Bain¹,

Fornasini²,

Evans

2005

CDM

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“…In particular, low quantities of Gamma-proteobacteria and high levels of Erysipelotrichi in human faecal microbiota are associated with hepatic steatosis 57 . Microbial and host enzymatic activities interact in choline's transformation into toxic methylamines, so trimethylamine that is produced by intestinal microbes can be further metabolized to trimethylamine-N-oxide in the liver 58,59 . These transformations may decrease the levels of bioavailable choline and are suggested to trigger non-alcoholic fatty liver disease (NAFLD) in mice 58 .…”

Section: Microbial Metabolism Of Cholinementioning

confidence: 99%

Functional interactions between the gut microbiota and host metabolism

Tremaroli

Bäckhed

2012

Nature

3,658

2,516

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Carbohydrates are important sources of energy for human and microbial cells. Human enzymes cannot degrade most complex carbohydrates and plant polysaccharides. Instead, the non-digestibleThe link between the microbes in the human gut and the development of obesity, cardiovascular disease and metabolic syndromes, such as type 2 diabetes, is becoming clearer. However, because of the complexity of the microbial community, the functional connections are less well understood. Studies in both mice and humans are helping to show what effect the gut microbiota has on host metabolism by improving energy yield from food and modulating dietary or the host-derived compounds that alter host metabolic pathways. Through increased knowledge of the mechanisms involved in the interactions between the microbiota and its host, we will be in a better position to develop treatments for metabolic disease.

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“…In previous studies to diagnose trimethylaminuric subjects, choline loading was used instead of trimethylamine (Marks et al, 1977;Spellacy et al, 1979;Brewster & Schedewie, 1983). Orally administered choline is degraded by gut microflora and TMA is liberated (De La Huerga & Popper, 1951;Prentiss et al, 1961). This is the basis for the diagnosis of affected homozygotes since they have a lowered ability to N-oxidize TMA; consequently a large amount of free TMA is excreted in the urine which is detected by gas-liquid chromatography.…”

Section: Discussionmentioning

confidence: 99%

Trimethylaminuria: The detection of carriers using a trimethylamine load test

Al-Waiz

Ayesh

Mitchell

et al. 1988

J of Inher Metab Disea

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A method potentially of value for investigating putative heterozygotes or carriers of trimethylaminuria by using a single oral dose of trimethylamine (TMA) is described. For healthy volunteers under normal dietary condition and following oral challenge with 300 mg and 600 mg TMA-base, over 90% of the urinary TMA was excreted in the form of TMA (93.6 +/- 1.6%). However, at a dose level of 900 mg TMA-base, there was clear evidence of saturation of the N-oxidation reaction as urinary TMA excretion declined to 77.2% (range 74.8-78.9) of the total dose of TMA. By contrast, in pedigree studies based upon propositi with trimethylaminuria, several parents were identified who showed clear evidence of saturation of the N-oxidation of TMA at the 600 mg TMA-base dose level, but not at 300 mg TMA-base or under normal dietary condition. In these individuals, the proportion of urinary TMA as trimethylamine N-oxide (TMAO) declined to (77.3 +/- 1.7%). Accordingly we propose that the oral administration of 600 mg TMA-base and the analysis of the following 0-8-h urine collection may be useful for the investigation of possible carriers of trimethylaminuria.

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The metabolism of choline by the germfree rat

Cited by 36 publications

References 9 publications

Trimethylamine: Metabolic, Pharmacokinetic and Safety Aspects

Trimethylamine: Metabolic, Pharmacokinetic and Safety Aspects

Functional interactions between the gut microbiota and host metabolism

Trimethylaminuria: The detection of carriers using a trimethylamine load test

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