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     Quick Explanation


    BT0430 is a phenylpyruvate:ferredoxin oxidoreductase gene in Bacteroides thetaiotaomicron that catalyses phenylalanine-to-phenylacetic acid (PAA) conversion; genetic deletion (Ξ”BT0430) abolished bacterial PAA production, lowered plasma PAA conjugates, and significantly attenuated steatosis and fibrosis in gnotobiotic mice [].


     Long Explanation


    What BT0430 is

    BT0430 encodes a phenylpyruvate:ferredoxin oxidoreductase in Bacteroides thetaiotaomicron VPI-5482, required for converting dietary phenylalanine into phenylacetic acid (PAA). When wild-type and markerless Ξ”BT0430 strains were cultured with phenylalanine, PAA was detected only in wild-type cultures, establishing BT0430 as necessary for this metabolic route [].

    Causal role in MASLD

    Germ-free C57BL/6N mice mono-colonised with Ξ”BT0430 vs wild-type B. thetaiotaomicron and fed a 21% protein LIDPAD diet for 12 weeks (n=8 vs 10) showed markedly reduced plasma phenylacetylglutamine (PAGly) and significantly lower composite SAF, steatosis, and fibrosis histological scores with the deletion strain (Mann-Whitney; unpaired t-test for PAGly) []. PAA and its host conjugate PAGln were also diet-dependent: protein restriction reduced caecal PAA only in microbiota-intact mice (t=-4.24, FDR=0.002), with a significant protein Γ— antibiotic interaction (t=-4.18, FDR=0.009) []. In a human ABOS obesity cohort (n=1,389), plasma PAGln was selectively elevated in the cardiometabolic MASLD subtype, though this cross-sectional association cannot establish causality [].

    Blindspots

    Only male mice were studied; PAA production within complex multi-species communities (other taxa may encode redundant homologues) was not tested; and human data lacked dietary intake and microbiome profiling. Disproving evidence would be any gnotobiotic experiment showing Ξ”BT0430 does not reduce hepatic phenotypes when replicated.



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    Updated: October 06, 2026

     Analysis Wizard



    Analysing BT0430 homolog prevalence across human gut metagenomes and correlating with plasma PAGln using PRJNA1528863 and ABOS metabolomics data.



     Hypothesis Graveyard


    BT0430 deletion was expected to abolish MASLD phenotypes via body-weight or glucose effects; instead steatosis worsened without weight or glucose tolerance changes, implicating direct hepatic PAA-conjugate signalling.

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    BT0430 Science Art

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