肠脑轴对胎儿肝胆疾病的影响

Mukesh Kumar Yadav, Zeeshan Ahmed Khan, Jing-Hua Wang, AbuZar Ansari
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引用次数: 0

摘要

肝胆系统对内源性分子的生物转化和处置至关重要。肝胆系统正常功能的任何损害都会导致一系列肝胆疾病(HBD),如肝硬化、脂肪肝、胆汁运动障碍、胆囊癌等。特别是在妊娠期,HBD 可能会导致孕产妇和胎儿的发病率和死亡率增加。母体 HBD 是胎儿生长的负担,使胎儿发育复杂化,并危及母亲的生命。在胎儿发育过程中,母体机制会受到多种因素(尤其是饮食)的严重干扰,从而影响胎儿的发育,增加日后患代谢性疾病的频率。此外,母体营养不足或营养过剩(尤其是高脂肪、高碳水化合物或富含蛋白质的饮食)会导致肠道激素(CCK、GLP-1 等)、微生物群代谢产物(SCFA、LPS、TMA 等)、神经递质(POMC、NPY 等)和肝胆信号传导(胰岛素抵抗、TNF-a、SREBPs 等)失调,从而对胎儿的发育产生重大影响。最近,生物治疗为治疗胎儿发育过程中的肝胆疾病以挽救母亲和胎儿的生命提供了新的视角。本综述重点探讨母体肝胆代谢信号受损如何通过肠脑轴介导疾病向胎儿传播。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Impact of Gut–Brain Axis on Hepatobiliary Diseases in Fetal Programming
The hepatobiliary system is vital for the biotransformation and disposition of endogenous molecules. Any impairment in the normal functioning of the hepatobiliary system leads to a spectrum of hepatobiliary diseases (HBDs), such as liver cirrhosis, fatty liver, biliary dyskinesia, gallbladder cancer, etc. Especially in pregnancy, HBD may result in increased maternal and fetal morbidity and mortality. Maternal HBD is a burden to the fetus’s growth, complicates fetal development, and risks the mother’s life. In fetal programming, the maternal mechanism is significantly disturbed by multiple factors (especially diet) that influence the development of the fetus and increase the frequency of metabolic diseases later in life. Additionally, maternal under-nutrition or over-nutrition (especially in high-fat, high-carbohydrate, or protein-rich diets) lead to dysregulation in gut hormones (CCK, GLP-1, etc.), microbiota metabolite production (SCFA, LPS, TMA, etc.), neurotransmitters (POMC, NPY, etc.), and hepatobiliary signaling (insulin resistance, TNF-a, SREBPs, etc.), which significantly impact fetal programming. Recently, biotherapeutics have provided a new horizon for treating HBD during fetal programming to save the lives of the mother and fetus. This review focuses on how maternal impaired hepatobiliary metabolic signaling leads to disease transmission to the fetus mediated through the gut–brain axis.
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