肠道稳态与脂质代谢交互作用在胃肠道动力中的调控机制

The Regulatory Mechanism of the Interaction between Intestinal Homeostasis and Lipid Metabolism in Gastrointestinal Motility

摘要: 肠道菌群与脂质代谢之间的交互作用在维持胃肠道动力和全身代谢稳态中发挥关键作用。肠道微生物通过代谢产物如短链脂肪酸、胆汁酸和芳香族氨基酸衍生物，与宿主模式识别受体如Toll样受体(Toll-like receptor; TLR)、NOD样受体(NOD-like receptor; NLR)、G蛋白偶联受体(G protein-coupled receptor; GPCR)互作，调控脂质合成、吸收与能量消耗。胆汁酸经菌群修饰后激活法尼醇X受体(Farnesoid X receptor; FXR)、G蛋白偶联胆汁酸受体5 (G protein-coupled bile acid receptor 5; TGR5)等受体，抑制肝脏脂质生成并促进能量代谢。菌群失调可破坏肠屏障，导致脂多糖(Lipopolysaccharide; LPS)易位，引发慢性炎症和脂代谢紊乱。免疫细胞如3型固有淋巴细胞(Innate Lymphoid Cell type 3; ILC3)、T细胞通过感知菌群信号调控脂质相关基因表达。该轴线的失衡与肥胖、高脂血症和糖尿病等代谢性疾病密切相关，靶向干预菌群–脂质代谢通路具有潜在治疗价值。

Abstract: The interaction between gut microbiota and lipid metabolism plays a crucial role in maintaining gastrointestinal motility and systemic metabolic homeostasis. The gut microbiota regulates lipid synthesis, absorption, and energy expenditure by interacting with host pattern recognition receptors such as Toll-like receptor (TLR), NOD-like receptor, (NLR), G protein-coupled receptor (GPCR), through metabolites such as short chain fatty acids, bile acids, and aromatic amino acid derivatives. Bile acids, modified by microbial communities, activate receptors such as Farnesoid X receptor (FXR) and Lipopolysaccharide (LPS), inhibit hepatic lipid production, and promote energy metabolism. Dysbiosis of the microbiota can disrupt the intestinal barrier, leading to LPS translocation, chronic inflammation, and lipid metabolism disorders. Immune cells such as Innate Lymphoid Cell type 3 (ILC3) and T cells regulate lipid related gene expression by sensing microbiota signals. The imbalance of this axis is closely related to metabolic diseases such as obesity, hyperlipidemia and diabetes, and targeted intervention of flora lipid metabolic pathway has potential therapeutic value.