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. 2024 Mar 20;15:1370658. doi: 10.3389/fimmu.2024.1370658

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Copyright © 2024 Niu, Zhou, Zogona, Xing, Wu, Chen, Cui, Liang and Xu

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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A. muciniphila regulating mechanisms associated with metabolic diseases. (1) Pasteurized A. muciniphila reduces glycerol and fatty acid levels and triglyceride (TG) production through inhibiting carbohydrate absorption. A. muciniphila cellular lysate upregulates serine protease inhibitor peptidase inhibitor clade 3G (SERPINA3G) expression in adipocytes and inhibits adipogenesis. (2) Activation of toll-like receptors 2 (TLR2) by Amuc _1100, an outer membrane protein of A. muciniphila, increases the thickness of the mucus layer and promotes the expression of tight junction proteins ZO-1, Occludin, and Claudin3. The enhancement of intestinal barrier function will hinder the insulin resistance induced by the activation of NF-KB/MAPKs signaling pathway caused by the combination of lipopolysaccharide (LPS) penetration and toll-like receptors 4 (TLR4). The glucagon-like protein P9 produced by A. muciniphila binds to the intercellular adhesion molecule 2 (ICAM-2) on the surface of L cells and activates phospholipase C (PLC), intracellular Ca²⁺ signaling, and CREB. P9 is involved in the secretion of GLP-1. Short- chain fatty acids (SCFAs) increased by A. muciniphila supplementation interact with free fatty acid receptor (FFAR) 2 and 3 on the surface of L cells to stimulate the secretion of GLP-1. (3) Pasteurized A. muciniphila inhibits the conversion of trimethylamine (TMA) to trimethylamine oxide (TMAO) by reducing the expression of hepatic flavin monooxygenase 3 (FMO3), and lowers the ratio of TAM/TAMO in plasma. A. muciniphila reduces the organism cholesterol (CHOL) and inflammation levels, indirectly reducing the risk of atherosclerosis and cardiovascular disease (CVD). (4) A. muciniphila indirectly decreases liver fat by regulating the level of free fatty acids (FFAs) in plasma. Supplementation with A. muciniphila increased the levels of L-aspartate in the gut-hepatic axis. L-Aspartate stimulate lipid oxidation and released energy by activating the hepatic LKB1-AMPK axis, thereby reducing liver fat accumulation. The figure was created using Figdraw.