Huang Huan, Huang Juan, Huang Wendi, Huang Nanqu, Duan Miao
Department of Pediatrics, Third Affiliated Hospital of Zunyi Medical University (The First People's Hospital of Zunyi), Zunyi, Guizhou, China.
Department of Pharmacology and Chemical Biology, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Front Nutr. 2023 Feb 21;10:1121213. doi: 10.3389/fnut.2023.1121213. eCollection 2023.
Breast milk jaundice (BMJ) is one of the main factors leading to interruption or early termination of breastfeeding. Interrupting breastfeeding to treat BMJ may increase the adverse consequences for infant growth and disease prevention. The Intestinal flora and metabolites are increasingly recognized as a potential therapeutic target in BMJ. First, dysbacteriosis can lead to a decrease in the metabolite short-chain fatty acids. At the same time, SCFA can act on specific G protein-coupled receptors 41 and 43 (GPR41/43), and a decrease in SCFA downregulates the GPR41/43 pathway, leading to a diminished inhibition of intestinal inflammation. In addition, intestinal inflammation leads to a decrease in intestinal motility and a large amount of bilirubin enters the enterohepatic circulation. Ultimately, these changes will result in the development of BMJ. In this review, we will describe the underlying pathogenetic mechanism of the intestinal flora effects on BMJ.
母乳性黄疸(BMJ)是导致母乳喂养中断或提前终止的主要因素之一。中断母乳喂养来治疗母乳性黄疸可能会增加对婴儿生长和疾病预防的不良后果。肠道菌群和代谢产物越来越被认为是母乳性黄疸潜在的治疗靶点。首先,菌群失调会导致代谢产物短链脂肪酸减少。同时,短链脂肪酸可作用于特定的G蛋白偶联受体41和43(GPR41/43),短链脂肪酸减少会下调GPR41/43通路,导致对肠道炎症的抑制减弱。此外,肠道炎症会导致肠道蠕动减慢,大量胆红素进入肠肝循环。最终,这些变化将导致母乳性黄疸的发生。在本综述中,我们将描述肠道菌群影响母乳性黄疸的潜在发病机制。