Clostridium butyricum upregulates GPR109A/AMPK/PGC-1α and ameliorates acute pancreatitis-associated intestinal barrier injury in mice.

Acute pancreatitis frequently causes intestinal barrier damage, which aggravates pancreatitis. Although Clostridium butyricum exerts anti-inflammatory and protective effects on the intestinal barrier during acute pancreatitis, the underlying mechanism is unclear. The G protein-coupled receptors 109 A (GPR109A) and adenosine monophosphate-activated protein kinase (AMPK)/ peroxisome proliferator-activated receptor-gamma coactivator 1 alpha (PGC-1α) signaling pathways can potentially influence the integrity of the intestinal barrier. Our study generated acute pancreatitis mouse models via intraperitoneal injection of cerulein and lipopolysaccharides. After intervention with Clostridium butyricum, the model mice showed reduced small intestinal and colonic intestinal barrier damage, dysbiosis amelioration, and increased GPR109A/AMPK/PGC-1α expression. In conclusion, Clostridium butyricum could improve pancreatic and intestinal inflammation and pancreatic injury, and relieve acute pancreatitis-induced intestinal barrier damage in the small intestine and colon, which may be associated with GPR109A/AMPK/PGC-1α.

Exploring the effect of Clostridium butyricum on lung injury associated with acute pancreatitis in mice by combined 16S rRNA and metabolomics analysis.

OBJECTIVES: Acute lung injury is a critical complication of severe acute pancreatitis (SAP). The gut microbiota and its metabolites play an important role in SAP development and may provide new targets for AP-associated lung injury. Based on the ability to reverse AP injury, we proposed that Clostridium butyricum may reduce the potential for AP-associated lung injury by modulating with intestinal microbiota and related metabolic pathways. METHODS: An AP disease model was established in mice and treated with C. butyricum. The structure and composition of the intestinal microbiota in mouse feces were analyzed by 16 S rRNA gene sequencing. Non-targeted metabolite analysis was used to quantify the microbiota derivatives. The histopathology of mouse pancreas and lung tissues was examined using hematoxylin-eosin staining. Pancreatic and lung tissues from mice were stained with immunohistochemistry and protein immunoblotting to detect inflammatory factors IL-6, IL-1ß, and MCP-1. RESULTS: C. butyricum ameliorated the dysregulation of microbiota diversity in a model of AP combined with lung injury and affected fatty acid metabolism by lowering triglyceride levels, which were closely related to the alteration in the relative abundance of Erysipelatoclostridium and Akkermansia. In addition, C. butyricum treatment attenuated pathological damage in the pancreatic and lung tissues and significantly suppressed the expression of inflammatory factors in mice. CONCLUSIONS: C. butyricum may alleviate lung injury associated with AP by interfering with the relevant intestinal microbiota and modulating relevant metabolic pathways.

Vitamin E in paediatric non-alcoholic fatty liver disease: a meta-analysis.

AIMS: There is currently no specific treatment for non-alcoholic fatty liver disease (NAFLD) in children, but recent studies have shown that vitamin E may be effective. Therefore, we conducted a meta-analysis of trials in which vitamin E was used to treat paediatric NAFLD. METHODS: We searched the PubMed, Embase, Scopus and Cochrane Library databases to identify related articles published prior to March 2020 that examined the effect of vitamin E for the treatment of paediatric NAFLD. RESULTS: The results showed that vitamin E significantly decreased low-density lipoprotein (LDL) and total cholesterol (TCHO) levels. However, no significant changes were found in other indicators, including body mass index (BMI), triglyceride (TG) levels, high-density lipoprotein (HLD) levels, fasting insulin levels, homeostatic model assessment (HOMA-IR), alanine transaminase (ALT) levels, aspartate aminotransferase (AST) levels, glutamate transpeptidase (GGT) levels, ballooning degeneration and fibrosis (P > 0.05). Although the P value of NAS was less than 0.05, the evidence was not strong enough. We also found that treatment with vitamin E significantly increased fasting glucose (FSG) levels if the intervention time was ≤12 months. CONCLUSIONS: Vitamin E therapy can improve blood lipids to some extent, but its effect on children's liver function and liver tissue is not apparent, and the finding that this therapy increases FSG levels still needs more research. SYSTEMATIC REVIEW REGISTRATION: PROSPERO CRD42020177663.