Small molecules produced or modified by gut microbiota that serve as key mediators of microbiome-host interactions. These metabolites translate microbial community composition into functional effects on host physiology, and their profiles are altered by metal exposure and dysbiosis.
Major Classes
- short chain fatty acids (butyrate, propionate, acetate): anti-inflammatory, barrier-protective, energy substrates for colonocytes.
- bile acid metabolism: microbial bile salt hydrolases (BSH) and 7-alpha-dehydroxylases convert primary to secondary bile acids; metal exposure depletes BSH-expressing bacteria.
- tmao: trimethylamine N-oxide, produced from dietary choline/carnitine by gut bacteria; pro-atherogenic.
- Tryptophan metabolites: indoles, kynurenines; modulate inflammation and gut brain axis signaling.
- butyrate: the single most-studied SCFA; histone deacetylase inhibitor with anti-cancer and anti-inflammatory properties.
Metal Interactions
- Heavy metals (cadmium, lead, arsenic, mercury) deplete SCFA-producing bacteria, reducing butyrate output.
- iron supplementation shifts metabolite profiles by favoring siderophore-producing pathogens over fermenters.
- zinc deficiency alters bile acid metabolism and tryptophan catabolism.
Connections
- gut metal microbiome — metals reshape the metabolite landscape
- short chain fatty acids — the most studied class of microbiome-derived metabolites
- dysbiosis — metabolite profile shifts are the functional readout of dysbiosis
- inflammation — metabolites mediate anti- and pro-inflammatory effects