Abstract: >Flavin containing monooxygenases (FMOs) are promiscuous enzymes known for metabolizing a wide range of exogenous compounds. In C. elegans, fmo-2 expression increases lifespan and healthspan downstream of multiple longevity-promoting pathways through an unknown mechanism. Here, we report that, beyond its classification as a xenobiotic enzyme, fmo-2 expression leads to rewiring of endogenous metabolism principally through changes in one carbon metabolism (OCM). These changes are likely relevant, as we find that genetically modifying OCM enzyme expression leads to alterations in longevity that interact with fmo-2 expression. Using computer modeling, we identify decreased methylation as the major OCM flux modified by FMO-2 that is sufficient to recapitulate its longevity benefits. We further find that tryptophan is decreased in multiple mammalian FMO overexpression models and is a validated substrate for FMO-2. Our resulting model connects a single enzyme to two previously unconnected key metabolic pathways and provides a framework for the metabolic interconnectivity of longevity-promoting pathways such as dietary restriction. FMOs are well-conserved enzymes that are also induced by lifespan-extending interventions in mice, supporting a conserved and important role in promoting health and longevity through metabolic remodeling.

I wish I understood what this means and how I could use it to my benefit. I’m more versed in psychology and chemistry than biology or biochemistry.

This is useful. At least now I know more about how riboflavin feeds into one carbon and transulferation pathways. Why FAD is as important as NAD.

This may be a backend of why dysregulation of transulferation pathways speed up aging, and why certain transulferation gene variants have much longer lifespans.

It ties in metabolism of NO2 for Nucleotides, h2s for transulferation, and one carbon, and why they should be kept in balance.

Touches on epigenetic quality control.

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Practice calorie restriction and live a longer life.