The gut microbiome as a target for prevention and treatment of hyperglycaemia in type 2 diabetes: from current human evidence to future possibilities.

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Term Occurence Count Dictionary
glucose intolerance 1 endocrinologydiseases
metabolic syndrome 1 endocrinologydiseases
metformin 22 endocrinologydiseasesdrugs
obesity 4 endocrinologydiseases

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Select Drug Character Offset Drug Term Instance
metformin 1692 treatment strategies that involve, or are based on, modification of gut microbiota (diet, probiotics, metformin and bariatric surgery). We go on to review some potential future gut-based glucose-lowering approaches
metformin 2037 components of probiotics, targeted delivery of propionate in the proximal colon, targeted delivery of metformin in the lower gut, faecal microbiota transplantation, and the incorporation of genetically modified bacteria
metformin 9147 B. vulgatus being the main producers of BCAAs. Interestingly, glucose-lowering treatments, such as metformin , can alter overall bacterial composition e.g. by increasing abundance of Lactobacillus and Escherichia
metformin 13043 the previously observed differences in the gut microbiota in diabetes could indeed be explained by metformin treatment. In line with previous studies [[10], [12]], Forslund and colleagues found that individuals
metformin 13202 [12]], Forslund and colleagues found that individuals with type 2 diabetes who were not treated with metformin had less bacteria from genera known to produce butyrate as compared with control participants without
metformin 13466 previously reported increase in Lactobacillus species among type 2 diabetes individuals results from metformin treatment [[11]]. Metformin-treated individuals were also observed to have increased abundance of Escherichia
metformin 13685 species in the gut, suggested to potentially contribute to the adverse gastrointestinal effects of metformin .Another recent study integrated data on insulin resistance, the gut microbiome and the fasting serum
metformin 17106 an understanding of individual responses to dietary interventions [[22]].The therapeutic effects of metformin are mediated by gut microbiotaThe primary site of action and the main glucose-lowering effects of metformin
metformin 17214 metformin are mediated by gut microbiotaThe primary site of action and the main glucose-lowering effects of metformin have been debated. However, important novel information has now emerged demonstrating that the primary
metformin 17400 demonstrating that the primary effects of the drug may reside in the gut; the pharmacological action of metformin was observed to include alterations in bile acid recirculation and gut microbiota, resulting in enhanced
metformin 17727 diabetes and 544 control participants without diabetes, stratified by treatment regiments, found that metformin had a significant effect on gut microbiota composition, such that individuals with type 2 diabetes who
metformin 17848 significant effect on gut microbiota composition, such that individuals with type 2 diabetes who were on metformin could be identified based on compositional changes in their gut microbiota [[11]]. Functionally, the
metformin 17977 based on compositional changes in their gut microbiota [[11]]. Functionally, the gut microbiota of metformin -treated individuals had increased potential to produce butyrate and propionate, while the untreated
metformin 18584 improve insulin sensitivity in type 2 diabetes [[25]]. Further, increased abundance of Escherichia in metformin -treated individuals has been functionally attributed to the enrichment of virulence factors and genes
metformin 18802 associated with gas metabolism, indicating involvement of this genus in the intestinal adverse effects of metformin . The work by Forslund et al thus suggests potential microbiota-mediated mechanisms behind both the therapeutic
metformin 18946 suggests potential microbiota-mediated mechanisms behind both the therapeutic and adverse effects of metformin [[11]].Additional evidence and mechanistic insights supporting a predominant action of metformin in
metformin 19043 of metformin [[11]].Additional evidence and mechanistic insights supporting a predominant action of metformin in the lower gut have recently been provided by clinical studies testing the response to delayed-release
metformin 19158 the lower gut have recently been provided by clinical studies testing the response to delayed-release metformin (MetDR) in healthy volunteers and participants with type 2 diabetes [[26], [27]]. The delayed release
metformin 19640 have demonstrated that MetDR has a glucose-lowering efficacy comparable with that of extended- release metformin but with a 40% increase in potency, thus allowing for lower doses of MetDR to be used [[27]]. In line
metformin 19880 trials demonstrated that MetDR resulted in glucose-lowering effects comparable with immediate-release metformin , despite significantly lower systemic exposure [[26]]. Large-scale Phase III clinical trials are now
metformin 20204 MetDR. In addition, whether MetDR affects the gut microbiota in a similar manner to immediate-release metformin is currently unknown and must be investigated.Bariatric surgery remodels the gut microbiota compositionBariatric
metformin 32213 treat type 2 diabetes. Importantly, recent data has demonstrated that the glucose-lowering effects of metformin are mediated by changes in the composition and function of gut microbiota. Several potential gut-targeting
Select Disease Character Offset Disease Term Instance
glucose intolerance 14931 diagnosed type 2 diabetes, and suggested that low abundance of this bacteria could be a biomarker for glucose intolerance [[8]]. More recently, A. muciniphila was observed to be decreased prior to the onset of type 2 diabetes
metabolic syndrome 26030 results [[41]]. In the first human study of 18 individuals, FMT from lean individuals to men with the metabolic syndrome resulted in significant improvements in peripheral insulin sensitivity along with an increase in butyrate-producing
obesity 7690 the much larger number of animal studies in the field. Similarly, separating the findings related to obesity or inflammation from those related to glycaemic traits is not straightforward. Therefore, this review
obesity 14592 elevated BCAAs in insulin resistance [[13], [14]].One specific bacteria that has been the focus of several obesity and type 2 diabetes studies is the mucus-colonising Akkermansia muciniphila. Zhang et al found A. muciniphila
obesity 24556 was surprisingly found to have an enhanced capacity to improve glucose metabolism in mouse models of obesity and diabetes. Further, a specific outer membrane protein of A. muciniphila, Amuc_1100, was found to
obesity 30087 observed a significant association between variation in the gene PLD1, which has been associated with obesity in African-American individuals, and the abundancy of Akkermansia [[48]]. Another GWAS found nine SNPs

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