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MEBO - UBIOME study 2018

'PRESS RELEASE'

NCT03582826
ClinicalTrials.gov

MEBO Gut Microbiome Study
"Microbial Basis of Systemic Malodor and PATM Conditions (PATM)"
Funded by uBiome Research Grant

"Microbial Basis of Systemic Malodor and PATM Conditions (PATM)"

Dynamics of the Gut Microbiota in
Idiopathic Malodor Production
& PATM

Started May 2018 - Ongoing

Current people sent kits : 100/100
3 kits per person

NO LONGER RECRUITING

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Metabolomic Profiling Study
NCT02683876

Start : Aug 2016
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Saturday, June 26, 2010

pubmed study : Flavin-containing monooxygenase-3: induction by 3-methylcholanthrene

A few years back, a group of toxicology researchers from the university of Toronto discovered accidentally that FMO3 could be induced in male mice by certain dioxides. It is currently taught that FMO3 is not inducible.

http://dmd.aspetjournals.org/content/36/12/2499.long

They have since investigated this finding further, with help from two world-renowned FMO3 experts (Krueger and Williams), and again repeated the findings. The latest paper found that 2 types of dioxins greatly increased FMO3 RNA induction, but this resulted in only modest increases of production of the actual FMO3 protein. Nevertheless it disproves that FMO3 cannot be induced, and perhaps could lead to finding safe ways of inducing FMO3 in humans. At the moment their research seems to be specific to male mice in particular, and not female mice, and could not be replicated in rats. It may be species specific. Also, induction is 'overclocking' an enzyme, so may not be a good long-term idea. It has not been tested in humans, and the research also only applies to fully potentially functioning FMO3 enzyme.
Flavin-containing monooxygenase-3: induction by 3-methylcholanthrene and complex regulation by xenobiotic chemicals in hepatoma cells and mouse liver.

Celius T, Pansoy A, Matthews J, Okey AB, Henderson MC, Krueger SK, Williams DE.

Department of Pharmacology and Toxicology, University of Toronto, Toronto, Canada M5S 1A8.

Abstract
Flavin-containing monooxygenases often are thought not to be inducible but we recently demonstrated aryl hydrocarbon receptor (AHR)-dependent induction of FMO mRNAs in mouse liver by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) (Celius et al., Drug Metab Dispos 36:2499, 2008). We now evaluated FMO induction by other AHR ligands and xenobiotic chemicals in vivo and in mouse Hepa1c1c7 hepatoma cells (Hepa-1). In mouse liver, 3-methylcholanthrene (3MC) induced FMO3 mRNA 8-fold. In Hepa-1 cells, 3MC and benzo[a]pyrene (BaP) induced FMO3 mRNA >30-fold. Induction by 3MC and BaP was AHR-dependent but, surprisingly, the potent AHR agonist, TCDD, did not induce FMO3 mRNA in Hepa-1 cells nor did chromatin immunoprecipitation assays detect recruitment of AHR or ARNT to Fmo3 regulatory elements after exposure to 3MC in liver or in Hepa-1 cells. However, in Hepa-1, 3MC and BaP (but not TCDD) caused recruitment of p53 protein to a p53 response element in the 5'-flanking region of the Fmo3 gene. We tested the possibility that FMO3 induction in Hepa-1 cells might be mediated by Nrf2/antioxidant response pathways but agents known to activate Nrf2 or to induce oxidative stress did not affect FMO3 mRNA levels. The protein synthesis inhibitor, cycloheximide (which causes "superinduction" of CYP1A1 mRNA in TCDD-treated cells) by itself caused dramatic upregulation (>300-fold) of FMO3 mRNA in Hepa-1 suggesting that cycloheximide prevents synthesis of a labile protein that suppresses FMO3 expression. Although FMO3 mRNA is highly induced by 3MC or TCDD in mouse liver and in Hepa-1 cells, FMO protein levels and FMO catalytic function showed only modest elevation.

http://www.ncbi.nlm.nih.gov/pubmed/20570689

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