Keep in mind the study was in mice, not humans.
Quotes from the paper :
Quote
"Our results indicate a major role for FMO3 in modulating glucose and lipid homeostasis in vivo"
Comment by me : This might lead to more FMO3 research.
Quote : (When mice had disabled FMO3 function)
Abstract paper Nov 2014 :
Flavin containing monooxygenase 3 exerts broad effects on glucose and lipid metabolism and atherosclerosis
Abstract Link
Full paper Link
Why do I think this is important to people with metabolic malodors ?
FMO3 deficiency is accepted as causing TMAU due to high levels of trimethylamine. However FMO3 oxidizes 1,000s of small sulfides and amines in humans and I believe that someone with FMO3 deficiency may be prone to overload of any FMO3 substrate, many of which are very smelly. So any FMO3 research is good for those who think they have 'FMO3 substrate malodor'. For those who feel they just have TMAU (i.e. only trimethylamine is an issue) then FMO3 research would be good for them too anyhow.
Comment by me : This might lead to more FMO3 research.
Quote : (When mice had disabled FMO3 function)
"... resulted in decreased circulating TMAO levels and atherosclerosis Surprisingly, we also observed significant decreases in hepatic lipids and in levels of plasma lipids, ketone bodies, glucose and insulin"
Comment by me : The abstract seems to be saying that mice made FMO3 deficient had reduced atherosclerosis, hepatic lipids and plasma lipids, ketones, glucose and insulin, which I presume all are a good thing.
Quote :
In vivo and in vitro results were consistent with the concept that the effects were mediated directly by FMO3 rather than TMA/TMAO; in particular
Comment by me :
Previously they had suggested there is a connection between CVD and TMAO, but now they are suggesting the connection is with FMO3 function, and that reduced FMO3 function not only means less atherosclerosis, but of many other chemicals associated with general health problems such as diabetes.
Quote :
The recessive disorder trimethylaminuria, due to loss of function mutations
of FMO3 gene, occurs at a frequency of about 1 in 10,000 in Caucasian populations (4). It will be
of interest to examine whether these individuals or obligate heterozygous individuals exhibit
alterations in lipid and glucose metabolism.
Quote :
The recessive disorder trimethylaminuria, due to loss of function mutations
of FMO3 gene, occurs at a frequency of about 1 in 10,000 in Caucasian populations (4). It will be
of interest to examine whether these individuals or obligate heterozygous individuals exhibit
alterations in lipid and glucose metabolism.
What does it mean for those with FMO3 malodor syndrome ?
It's not much comfort for those with FMO3 deficiency malodors, except perhaps you may have some protection from heart disease or diabetes ? (if the hypothesis was correct). However it should lead to much more research into FMO3, which up until now was a very neglected enzyme with almost no research or interest. This research project itself must have cost a bit (no problem with funding), and it one of about 5 papers with this line of study over the last year or so.
Abstract paper Nov 2014 :
Flavin containing monooxygenase 3 exerts broad effects on glucose and lipid metabolism and atherosclerosis
Abstract Link
Full paper Link
Why do I think this is important to people with metabolic malodors ?
FMO3 deficiency is accepted as causing TMAU due to high levels of trimethylamine. However FMO3 oxidizes 1,000s of small sulfides and amines in humans and I believe that someone with FMO3 deficiency may be prone to overload of any FMO3 substrate, many of which are very smelly. So any FMO3 research is good for those who think they have 'FMO3 substrate malodor'. For those who feel they just have TMAU (i.e. only trimethylamine is an issue) then FMO3 research would be good for them too anyhow.
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