{"title":"高甘油三酯血症调节的肠道微生物群以tlr4依赖的方式促进溶血磷脂酰胆碱的产生，加重急性胰腺炎","authors":"Xiaofan Song, Lei Qiao, Xina Dou, Jiajing Chang, Xiaonan Zeng, Tianjing Deng, Ge Yang, Peiyun Liu, Cheng Wang, Qinhong Xu, Chunlan Xu","doi":"10.1002/imt2.70003","DOIUrl":null,"url":null,"abstract":"<p>Hypertriglyceridemia (HTG) can lead to the disorder of gut microbiota in mice, resulting in the increase of endotoxin content. HTG can also aggravate the damage of intestinal barrier function and intestinal bacterial translocation in acute pancreatitis (AP) mice. Toll-like receptor 4 gene <i>(Tlr4)</i> knockout can significantly reduce gut permeability and endotoxin invasion in AP mice. In addition, HTG-modulated gut microbiota could up-regulate glycerophospholipid metabolism and increase lysophosphatidylcholine (LysoPC) content in a TLR4-dependent manner, thereby aggravating pancreatic injury in AP.\n\n <figure>\n <div><picture>\n <source></source></picture><p></p>\n </div>\n </figure></p>","PeriodicalId":73342,"journal":{"name":"iMeta","volume":"4 1","pages":""},"PeriodicalIF":23.7000,"publicationDate":"2025-02-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/imt2.70003","citationCount":"0","resultStr":"{\"title\":\"Hypertriglyceridemia-modulated gut microbiota promotes lysophosphatidylcholine generation to aggravate acute pancreatitis in a TLR4-dependent manner\",\"authors\":\"Xiaofan Song, Lei Qiao, Xina Dou, Jiajing Chang, Xiaonan Zeng, Tianjing Deng, Ge Yang, Peiyun Liu, Cheng Wang, Qinhong Xu, Chunlan Xu\",\"doi\":\"10.1002/imt2.70003\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p>Hypertriglyceridemia (HTG) can lead to the disorder of gut microbiota in mice, resulting in the increase of endotoxin content. HTG can also aggravate the damage of intestinal barrier function and intestinal bacterial translocation in acute pancreatitis (AP) mice. Toll-like receptor 4 gene <i>(Tlr4)</i> knockout can significantly reduce gut permeability and endotoxin invasion in AP mice. In addition, HTG-modulated gut microbiota could up-regulate glycerophospholipid metabolism and increase lysophosphatidylcholine (LysoPC) content in a TLR4-dependent manner, thereby aggravating pancreatic injury in AP.\\n\\n <figure>\\n <div><picture>\\n <source></source></picture><p></p>\\n </div>\\n </figure></p>\",\"PeriodicalId\":73342,\"journal\":{\"name\":\"iMeta\",\"volume\":\"4 1\",\"pages\":\"\"},\"PeriodicalIF\":23.7000,\"publicationDate\":\"2025-02-11\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://onlinelibrary.wiley.com/doi/epdf/10.1002/imt2.70003\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"iMeta\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://onlinelibrary.wiley.com/doi/10.1002/imt2.70003\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q1\",\"JCRName\":\"MICROBIOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"iMeta","FirstCategoryId":"1085","ListUrlMain":"https://onlinelibrary.wiley.com/doi/10.1002/imt2.70003","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"MICROBIOLOGY","Score":null,"Total":0}
Hypertriglyceridemia-modulated gut microbiota promotes lysophosphatidylcholine generation to aggravate acute pancreatitis in a TLR4-dependent manner
Hypertriglyceridemia (HTG) can lead to the disorder of gut microbiota in mice, resulting in the increase of endotoxin content. HTG can also aggravate the damage of intestinal barrier function and intestinal bacterial translocation in acute pancreatitis (AP) mice. Toll-like receptor 4 gene (Tlr4) knockout can significantly reduce gut permeability and endotoxin invasion in AP mice. In addition, HTG-modulated gut microbiota could up-regulate glycerophospholipid metabolism and increase lysophosphatidylcholine (LysoPC) content in a TLR4-dependent manner, thereby aggravating pancreatic injury in AP.
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