Role of intestinal microbiota and metabolites on gut homeostasis and human diseases.

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Term Occurence Count Dictionary
Insulin 1 endocrinologydiseasesdrugs
hyperglycemia 1 endocrinologydiseases
metabolic syndrome 3 endocrinologydiseases
obesity 9 endocrinologydiseases
prednisone 2 endocrinologydiseasesdrugs

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Select Drug Character Offset Drug Term Instance
Insulin 97138 in common are believed to be relevant to insulin resistance, lipotoxicity, and inflammation [[171]]. Insulin resistance is a multi-organ manifestation as observed at the level of the liver, muscle and adipose
prednisone 93218 pathogens in immunocompromised hosts [[199]]. Among all the immunosuppressant drugs examined, only prednisone and mycophenolate mofetil showed a dose-dependent association with microbial colonization of oral cavity.
prednisone 93350 mofetil showed a dose-dependent association with microbial colonization of oral cavity. In particular, prednisone dose was found to positively correlate with the prevalence of two genera Klebsiella and Acenitobacter
Select Disease Character Offset Disease Term Instance
hyperglycemia 96977 linked up with ectopic fat accumulation, especially in the liver. T2D is characterized by persistent hyperglycemia . Pathophysiologic mechanisms of NAFLD and T2D in common are believed to be relevant to insulin resistance,
metabolic syndrome 77425 their effector IL-18 can negatively regulate NAFLD/NASH progression as well as multiple aspects of metabolic syndrome by modulating the gut microbiota [[168]]. Alterations in the gut microbiota configuration in mice are
metabolic syndrome 78130 impairment in NLRP3 and NLRP6 inflammasome sensing, may govern the propensity for development of multiple metabolic syndrome -associated abnormalities such as NAFLD-NASH progression [[168]]. The above findings would shed light
metabolic syndrome 88029 over-numbered E. coli) and the ensuing chronic inflammation, which in turn leads to manifestation of metabolic syndrome [[187], [190]].Investigation with MyD88−/− NOD mice also supports the aforementioned rational that
obesity 49189 microbiota and host, which regulates gut barrier function and other physiological functions during obesity and type 2 diabetes (T2D). Furthermore, merely viable A. muciniphila is able to exert the above-described
obesity 65426 of gut microbiota on the peripheral tissues beyond the gut. CNS: central nervous systemDiabetes and obesity It is thought that commensals are able to exert crucially biological actions on their host tissues, ranging
obesity 65908 gut inflammation, which may contribute to various diseases including infectious enterocolitis, IBD, obesity , diabetes, irritable bowel syndrome, small intestinal bacterial overgrowth, hepatic fibrosis, food intolerances
obesity 72719 needed for the design and development of novel disease preventative or therapeutic regimen.T2D and obesity Apart from T1D, extensive studies show that the intestine microbes affect host energy harvest in mammals,
obesity 72873 intestine microbes affect host energy harvest in mammals, suggesting a link of gut microbiota with obesity [[155]]. Firmicutes, Bacteroidetes, Actinobacteria and Proteobacteria are known to dominate the human
obesity 73335 siblings which are homozygous for a mutation in the leptin gene with the resultant phenotype of severe obesity [[158]]. Analogous to human, Firmicutes and Bacteroidetes are predominant bacterial phyla in healthy
obesity 75095 bacterial fragments could be promising targets to preventing/or inverting the incidence of diabetes and obesity [[161]]. This finding also broadens the avenue for treatment of metabolic disorders using probiotics
obesity 77850 hepatic TNF-α expression that promotes NASH progression. Moreover, exacerbation of hepatic steatosis and obesity were observed while inflammasome-lacking mice were co-housed with wild-type controls. Taken together,
obesity 78432 auto-inflammatory and metabolic disorders that are seemingly irrelevant. Analogous to metabolic disorders (i.e. obesity ), an increased prevalence of the Phylum Firmicutes is definitive of gut dysbiosis following the onset

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