Carnosine, and its derivative anserine, are known to function as anti-oxidants and putative neurotransmitters. They are especially rich in the breast muscle (Musculus pectoralis superficialis, MPS) of chickens. To clarify whether the concentrations of carnosine and anserine are altered by dietary management, the effect of oral administration of their constituent, b -alanine ( b -Ala), was determined in the MPS and brains of chickens. Birds were orally administered b -Ala (22 mmol/kg) twice a day for five consecutive days (from 2 to 6 days old). In the MPS, carnosine was increased by b -Ala, whereas anserine and taurine were decreased. The concentrations of other free amino acids in the MPS were also modified by b -Ala. In the brain, the oral administration of b -Ala increased anserine and carnosine and decreased taurine, but caused no changes to other free amino acid concentrations. These results suggest that orally administered b -Ala increases carnosine concentrations in both the MPS and brains of chickens. However, the effects of b -Ala on other concentrations differ depending on the tissues.

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L-amino acid oxidase (LAAO) is a metabolic enzyme that converts L-amino acids into ketoacids, ammonia, and hydrogen peroxide (H 2 O 2 ). The generated H 2 O 2 has previously been shown to have antibacterial and gut microbiota-modulatory properties in LAO1 knock-out (KO) mice. Since most microbial metabolites reach the liver through the portal vein, we examined gut-liver interactions in LAO1 KO mice. We found lower total cholesterol levels, higher glutamic pyruvic transaminase (GPT) levels in the serum, and higher pro-inflammatory cytokine mRNA expression in the liver tissue. In wild-type (WT) mice, LAO1 was expressed in gut tissues (ileum and colon). Microbiome analysis revealed that the abundance of some bacteria was altered in LAO1 KO mice. However, short-chain fatty acid (SCFAs) levels in cecal feces and gut permeability did not change. Fecal microbiota transplantation (FMT) revealed that feces from LAO1 KO mice slightly stimulated pro-inflammatory cytokine expression in the liver. During metabolomic analysis, 5-aminolevulinic acid (5-ALA) was the only metabolite found to be significantly upregulated in the portal and abdominal veins of the LAO1 KO mice. Intraperitoneal administration of 5-ALA to WT mice significantly increased IL-6 mRNA expression in the liver. These observations suggest that gut LAO1 plays a role in regulating 5-ALA production and that a high level of 5-ALA stimulates the liver to increase pro-inflammatory cytokine expression by disrupting LAO1 in mice.

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