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On May 10, the international academic journal " Cellular and Molecular Gastroenterology and Hepatology " published by the American Gastroenterological Association published an online publication of Li The latest collaborative research result of Yu's group and Fan Jiangao's group of Xinhua Hospital, Shanghai Jiaotong University School of Medicine, "Sodium butyrate supplementation inhibits hepatic steatosis by stimulating liver kinase B1 and insulin-induced gene", the study confirmed that butyrate, a metabolite of intestinal flora Sodium plays an important role in improving liver steatosis, and reveals a new mechanism that ultimately inhibits lipid synthesis by activating liver kinase B1 (LKB1) and endoplasmic reticulum anchoring protein Insig
Hepatic steatosis is a characteristic pathological change of non-alcoholic fatty liver disease.
The research group of Li Yu and the research group of Fan Jiangao of Xinhua Hospital Affiliated to Shanghai Jiaotong University School of Medicine jointly cultivated Ph.
Researcher Li Yu has long been engaged in the research of diabetes and non-alcoholic fatty liver disease
The research was supported and helped by researchers Gao Daming and Ji Hongbin from the Center for Excellence in Molecular Cell Science, Chinese Academy of Sciences, and Li Jia and Li Jingya from the Shanghai Institute of Materia Medica, Chinese Academy of Sciences
Research paper link: https://
Schematic diagram of the mechanism of intestinal flora metabolite butyric acid regulating liver lipid metabolism and improving liver lipid changes in mice
The butyric acid produced by the intestinal flora enters the liver through the portal vein, activates the LKB1-AMPK-Insig pathway, inhibits the transcription activity of SREBP-1c, thereby down-regulates the expression of lipid synthesis genes, reduces the level of lipid deposition in liver cells, and improves fatty liver
