ArticlePoultry science2026
Gut microbiota-derived taurolithocholic acid modulates myofiber-type switching via p38 MAPK/PGC-1α signaling underlying breed differences between Arbor Acres and Taoyuan chickens.
Article in Poultry science, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
It is well-established that the gut microbiota plays a crucial role in skeletal muscle development and homeostasis. However, the contribution of the gut microbiome to the distinct meat quality phenotypes observed between fast-growing commercial broilers and slow-growing local chicken breeds remains poorly understood. Therefore, this study aims to elucidate how the gut microbiota modulates pectoral muscle development by comparing muscle growth phenotypes and gut microbiome dynamics across these breeds. Using the fast-growing commercial Arbor Acres (AA) broiler and the slow-growing local breed Taoyuan (TY) chicken as models, we investigated how breed-specific gut microbiota modulate pectoral muscle fiber composition. AA broilers exhibited faster muscle growth but lower oxidative type I fiber proportion than TY chickens. While small intestinal microbiota succession was similar, cecal communities diverged markedly between breeds. Integrated metagenomic sequencing and metabolomics revealed that cecal Phocaeicola dorei abundance was strongly correlated with serum taurolithocholic acid (TLCA) levels and type I fiber content, especially in TY chickens, which prompted the selection of TLCA for functional validation. Reciprocal intestinal microbiota transplantation (IMT) shifted recipient muscle fiber phenotypes toward those of donors, confirming a causal role of the cecal microbiota. Furthermore, in vitro assays using AA-derived myoblasts demonstrated that TLCA promotes mitochondrial biogenesis and type I fiber formation by enhancing p38 MAPK phosphorylation and PGC-1α activation; this effect was abolished by the p38 inhibitor SB203580. Our study demonstrated that gut microbiota-derived TLCA modulates muscle fiber type transformation via the p38 MAPK/PGC-1α signaling pathway. This finding reveals an intricate mechanism whereby the gut microbiota regulates host muscle development through a metabolite-signaling axis, providing critical insights into the gut microbe-myofiber relationship.
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