Causal Relationship between Diet-Induced Gut Microbiota Changes and Diabetes: A Novel Strategy to Transplant Faecalibacterium prausnitzii in Preventing Diabetes

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hyperglycemia 2 endocrinologydiseases
metabolic syndrome 6 endocrinologydiseases
obesity 6 endocrinologydiseases

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hyperglycemia 15956 tissue, pancreatic progenitors, and intestinal stem cells into insulin-producing cells and ameliorates hyperglycemia [[135],[136]]. In addition, exogenous treatment of Ex-4 also leads to increased insulin secretion in
hyperglycemia 16923 more obviously heavier and significantly higher in GSIS. Moreover, Epac1−/− mice developed severe hyperglycemia with increased β-cell apoptosis and insulitis after type1 and immune model of diabetes using the multiple
metabolic syndrome 4908 [[10],[11],[12]], autoimmune disorders [[13],[14],[15]], inflammatory bowel diseases [[16],[17],[18]], metabolic syndrome [[19],[20],[21],[22],[23],[24],[25],[26],[27],[28]] and neurodegenerative diseases [[29],[30],[31],[32],[33]].
metabolic syndrome 16411 [[137]]. The critical experiment to show the importance of Epac 1 in mediating the GLP-1 signal and metabolic syndrome and diabetes was performed using the genetically engineered Epac1-deficient mice and embryonic stem
metabolic syndrome 17160 streptozotocin (MLDS; 40 mg/kg) treatment than Epac1+/+ mice. Interestingly, Epac1−/− mice also showed metabolic syndrome , with an increased respiratory exchange ratio and plasma triglyceride, and more severe diet-induced
metabolic syndrome 30662 [[217]] investigated the effects of infusing the gut microbiota from lean donors to male recipients with metabolic syndrome . In this study, the team substantiated the human colonization with F. prausnitzii used as a probiotic;
metabolic syndrome 32106 autoimmunity. Transplantation of intestinal microbiota especially F. prausnitzii from a normal individual to metabolic syndrome subjects, especially diabetic persons, is able to synthesize abundant quantity of butyrate, which stabilizes
metabolic syndrome 35689 diabetes, and obesity. In addition, the secretion of gut hormones (incretins ghrelin, amylin) can affect metabolic syndrome and diabetes [[19],[34],[35]]. IEC, intestinal epithelial cell; GLP-1, glucagon-like peptide-1; GIP,
obesity 14638 phenotypes of mice with the deletion of GPR41 and GPR43 presented altered chronic inflammation and obesity markers, which suggested that these GPCRs are important regulators of chronic inflammation in the gut,
obesity 14826 inflammation in the gut, respiratory tract and skeletal system and metabolic dysregulation leading to obesity [[131]]. Binding of ligands to GPR41 may trigger secretion of glucagon-like peptide 1 (GLP-1) and lead
obesity 17279 with an increased respiratory exchange ratio and plasma triglyceride, and more severe diet-induced obesity with insulin resistance, which may contribute to β-cell dysfunction and insulin secretion. Nevertheless,
obesity 18905 DiabetesGut microbiota compositions are connected with various hallmarks of metabolic dysfunctions, including obesity , and type-2 diabetes. Studies suggest that gut microbes contribute to the onset of the low-grade inflammation
obesity 30169 of low-grade inflammation. An elevated level of butyrate is considered to inhibit the diet-induced obesity [[216]] and cause suppression of inflammatory reactions [[199]]. Altogether, butyrate alone did not
obesity 35598 peripheral organs, leading to increased adiposity, chronic inflammation, oxidative stress, diabetes, and obesity . In addition, the secretion of gut hormones (incretins ghrelin, amylin) can affect metabolic syndrome

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