The Relationship between Frequently Used Glucose-Lowering Agents and Gut Microbiota in Type 2 Diabetes Mellitus.

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acarbose 17 endocrinologydiseasesdrugs
diabetes mellitus 11 endocrinologydiseases
hyperglycemia 3 endocrinologydiseases
hypoglycemia 1 endocrinologydiseases
metabolic syndrome 1 endocrinologydiseases
metformin 44 endocrinologydiseasesdrugs
obesity 3 endocrinologydiseases
type 2 diabetes mellitus 2 endocrinologydiseases

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acarbose 12718 predictor of diabetic cardiovascular events [[47], [48]]. As a classical α-glucosidase inhibitor, acarbose lowers postprandial blood glucose levels by delaying glucose absorption, as it inhibits the enzyme that
acarbose 13185 noninferiority clinical trial recruiting Chinese patients newly diagnosed with T2DM, treatment with acarbose as initial therapy showed similar glucose-lowering efficacy to that of metformin [[50]]. Therefore,
acarbose 13294 as initial therapy showed similar glucose-lowering efficacy to that of metformin [[50]]. Therefore, acarbose is an effective and safe antidiabetic agent, especially for the control of postprandial hyperglycemia.
acarbose 13425 safe antidiabetic agent, especially for the control of postprandial hyperglycemia. The major cause of acarbose side effects (e.g., diarrhea, flatulence, and abdominal distention) is the increased delivery of oligosaccharides
acarbose 13692 effects can be ameliorated by gradual upward dose titration [[29]]. Previous studies indicated that acarbose treatment could reduce the risk of cardiovascular events in diabetic patients [[51]–[54]]. The detailed
acarbose 13956 protective function are only partially understood [[55]], but they can be attributed to the ability of acarbose to neutralize oxidative stress by increasing H2 production in the GI tract (GIT) [[56]]. However, the
acarbose 14145 [[56]]. However, the results of Chang et al. did not support a cardiovascular protective effect of acarbose compared to metformin in Taiwan populations [[57]].A series of recent clinical trials clarified the
acarbose 14275 in Taiwan populations [[57]].A series of recent clinical trials clarified the relationship between acarbose and gut microbiota. For example, in a clinical study, 95 Chinese T2DM patients were distributed into
acarbose 14422 clinical study, 95 Chinese T2DM patients were distributed into 2 groups; one group was treated with acarbose while the other was not. At baseline, diabetic patients showed lower levels of Bifidobacterium longum
acarbose 14636 higher levels of Enterococcus faecalis than healthy volunteers [[55]]. After 4 weeks of treatment, acarbose -treated patients showed increased Bifidobacterium longum and decreased lipopolysaccharide and prothrombin
acarbose 14815 lipopolysaccharide and prothrombin activator inhibitor-1 levels [[55]]. These results suggest that acarbose treatment could alter gut microbiota and reduce the levels of inflammatory cytokines in diabetic patients.
acarbose 15053 double-blind, controlled crossover trial recruiting prediabetic Chinese individuals demonstrated that acarbose treatment significantly altered the diversity and composition of gut microbiota [[58]]. In addition,
acarbose 15194 the diversity and composition of gut microbiota [[58]]. In addition, Gu et al. [[23]] revealed that acarbose could regulate the gut microbiota of T2DM patients, thereby modulating bile acid metabolism and contributing
acarbose 15925 individuals with impaired glucose tolerance. The underlying mechanism for this effect might be that acarbose increases the fermentation of insoluble fibers in the colon [[25]]. Similarly, a clinical study showed
acarbose 16096 [[25]]. Similarly, a clinical study showed that butyrate production is significantly increased during acarbose treatment, whereas the production of acetate and propionate is significantly decreased [[26]].The beneficial
acarbose 16225 the production of acetate and propionate is significantly decreased [[26]].The beneficial effects of acarbose on diabetes mellitus, such as reduction of inflammatory cytokines and regulation of SCFA levels, can
acarbose 16479 microbiota. However, whether there is an association between the cardiovascular protective action of acarbose and gut microbiota is not yet clear.4. Glucagon-Like Peptide-1 (GLP-1) and Gut MicrobiotaEndocrine peptides
metformin 3242 botulinum E3 str. Alaska E43, and Clostridium thermocellum DSM 1313) in T2DM patients. Treatment with metformin affects gut microbiota, and thus, it might be an important confounder in the above studies. Gut microbiota
metformin 5562 transported into cells by organic cation transporters (OCT) [[29], [30]]. The mechanism of action of metformin is not yet fully understood. In an experimental study on mice with alanine knock-in mutations in both
metformin 5747 knock-in mutations in both acetyl-CoA carboxylase (Acc) 1 (Ser79) and Acc2 (Ser212), treatment with metformin reduced hepatic lipogenesis and lipid accumulation via activating AMPK and inhibited both Acc1 and Acc2,
metformin 5939 inhibited both Acc1 and Acc2, thereby increasing insulin sensitivity [[31]]. Duca et al. [[32]] found that metformin could activate duodenal mucosal AMPK and attenuate hepatic glucose production in a rat model of high-fat
metformin 6111 glucose production in a rat model of high-fat diet (HFD). In addition, Miller et al. [[33]] found that metformin lowers the fasting glucose level by inhibiting glucagon-stimulated cyclic adenosine monophosphate production,
metformin 6394 glucagon-stimulated glucose output. Metformin was also found to alter intestinal microbiota [[34]].Currently, metformin is the first-line treatment for T2DM and is recommended by the American Diabetes Association and the
metformin 6742 levels, improve lipid profiles, and promote modest weight loss. An extended-release formulation of metformin that has fewer gastrointestinal (GI) side effects, for example, diarrhea, anorexia, nausea, and metallic
metformin 6935 nausea, and metallic taste, is also available [[21], [29]]. About 30% of the patients treated with metformin report suffering from GI adverse effects [[1]]. In a previous clinical study in which 360 T2DM patients
metformin 7089 [[1]]. In a previous clinical study in which 360 T2DM patients were administered a new prescription of metformin for 3 months, about 88% of the participants reported single or multiple GI symptoms, including diarrhea,
metformin 7269 multiple GI symptoms, including diarrhea, heartburn, and nausea [[36]]. Possible underlying mechanisms for metformin adverse effects include stimulation of intestinal serotonin secretion, changes in incretin and glucose
metformin 7439 secretion, changes in incretin and glucose metabolism, bile salt malabsorption, and high intestinal metformin concentrations after oral administration [[37]]. Since OCT1 is involved in the absorption of metformin
metformin 7542 metformin concentrations after oral administration [[37]]. Since OCT1 is involved in the absorption of metformin from the intestinal lumen, its inhibition results in increased metformin intolerance [[37]]. Recent
metformin 7615 involved in the absorption of metformin from the intestinal lumen, its inhibition results in increased metformin intolerance [[37]]. Recent data illustrated that delayed-release metformin performs its action predominantly
metformin 7690 inhibition results in increased metformin intolerance [[37]]. Recent data illustrated that delayed-release metformin performs its action predominantly in the intestine, so it is considered to be safe for T2DM patients
metformin 8089 nearly 300 times higher than its plasma concentration [[39]]. Thus, the intestine is the major site of metformin exposure and is responsible for its glucose-lowering effect [[38]]. In 1984, Bonora et al. [[40]] found
metformin 8238 glucose-lowering effect [[38]]. In 1984, Bonora et al. [[40]] found that intravenous administration of metformin did not improve glucose metabolism compared to oral administration, which suggests the importance of
metformin 8406 administration, which suggests the importance of the intestine in the regulation of glucose metabolism by metformin . Metformin was found to increase the life span of Caenorhabditis elegans cocultured with Escherichia
metformin 8620 coli by altering microbial folate and methionine metabolism [[41]], which suggests that the effects of metformin on aging in nematodes are microbiota dependent. Recently, the relationship between metformin and the
metformin 8713 effects of metformin on aging in nematodes are microbiota dependent. Recently, the relationship between metformin and the gut has been comprehensively reviewed [[21]]; researchers indicated that metformin can affect
metformin 8804 between metformin and the gut has been comprehensively reviewed [[21]]; researchers indicated that metformin can affect the gut microenvironment by modulating glucose uptake and utilization, increasing glucagon-like
metformin 9028 peptide-1 (GLP-1) and bile acid levels and altering gut microbiota. In conclusion, the interaction between metformin and gut microbiota may contribute to the pleiotropic effects of metformin.A large body of evidence confirms
metformin 9102 conclusion, the interaction between metformin and gut microbiota may contribute to the pleiotropic effects of metformin .A large body of evidence confirms the effects of metformin on intestinal microbiota. The abundance of
metformin 9161 contribute to the pleiotropic effects of metformin.A large body of evidence confirms the effects of metformin on intestinal microbiota. The abundance of Akkermansia muciniphila was found to be decreased in obesity
metformin 9586 muciniphila [[43], [44]] and Clostridium cocleatum [[43]] increased significantly in HFD-fed mice after metformin treatment. The higher abundance of Akkermansia muciniphila was involved in maintaining mucin layer integrity
metformin 9871 SCFA-producing bacteria in human and animal guts [[45], [46]]. It is suggested that the effects of metformin on the abundance of these species may indirectly contribute to its modulatory effects on glucose metabolism
metformin 10073 glucose metabolism and other metabolic processes. These results suggest that the therapeutic effect of metformin might be partially mediated by the intestinal tract.Forslund et al. [[1]] found that metformin-treated
metformin 10168 effect of metformin might be partially mediated by the intestinal tract.Forslund et al. [[1]] found that metformin -treated T2DM patients exhibited decreased abundances of Intestinibacter spp. and increased abundances
metformin 10525 old women with T2DM, impaired glucose tolerance, or normal glucose tolerance, patients treated with metformin showed different gut microbial composition than those who were not treated with metformin [[12]]. Napolitano
metformin 10615 treated with metformin showed different gut microbial composition than those who were not treated with metformin [[12]]. Napolitano et al. also evaluated T2DM with and without metformin monotherapy to characterize
metformin 10688 who were not treated with metformin [[12]]. Napolitano et al. also evaluated T2DM with and without metformin monotherapy to characterize the gut-based mechanisms of metformin, and their results showed that Adlercreutzia
metformin 10754 also evaluated T2DM with and without metformin monotherapy to characterize the gut-based mechanisms of metformin , and their results showed that Adlercreutzia spp. were significantly elevated in fecal samples of metformin-treated
metformin 10862 metformin, and their results showed that Adlercreutzia spp. were significantly elevated in fecal samples of metformin -treated patients [[30]]. Wu et al. [[24]] found that the altered microbiota mainly belonged to the phyla
metformin 11183 Intestinibacter spp., as well as a significant increase in fecal propionate and butyrate concentrations in the metformin group. A possible underlying mechanism for metformin-microbiota interaction is regulating the expression
metformin 11236 propionate and butyrate concentrations in the metformin group. A possible underlying mechanism for metformin -microbiota interaction is regulating the expression of genes encoding for metalloproteins in gut bacteria.
metformin 11396 expression of genes encoding for metalloproteins in gut bacteria. These results demonstrate the influence of metformin on gut microbial diversity and the role of the intestine in the glucose-lowering effect of metformin.Unfortunately,
metformin 11497 metformin on gut microbial diversity and the role of the intestine in the glucose-lowering effect of metformin .Unfortunately, alteration of gut microbiota by metformin may contribute to its GI intolerance [[21]].
metformin 11554 intestine in the glucose-lowering effect of metformin.Unfortunately, alteration of gut microbiota by metformin may contribute to its GI intolerance [[21]]. Greenway et al. [[27]] reported a case in which a 30-year-old
metformin 11897 extract for 8 weeks. This patient exhibited balanced glycemic control and alleviated GI side effects of metformin . In addition, Burton et al. [[28]] found that the combination of metformin with GI microbiome modulator
metformin 11972 alleviated GI side effects of metformin. In addition, Burton et al. [[28]] found that the combination of metformin with GI microbiome modulator (GIMM) in T2DM patients who experienced GI intolerance to metformin resulted
metformin 12069 of metformin with GI microbiome modulator (GIMM) in T2DM patients who experienced GI intolerance to metformin resulted in better glucose tolerance compared to placebo and significantly improved fasting glucose
metformin 12289 These results demonstrate that a safe dietary supplement may improve the efficacy and tolerability of metformin , possibly through the alteration of gut microbiota. Thus, gut microbiota may serve as a novel approach
metformin 12415 through the alteration of gut microbiota. Thus, gut microbiota may serve as a novel approach to alleviate metformin adverse effects and consequently improve patient compliance.3. The Effect of Acarbose on Gut Microbiota
metformin 13265 T2DM, treatment with acarbose as initial therapy showed similar glucose-lowering efficacy to that of metformin [[50]]. Therefore, acarbose is an effective and safe antidiabetic agent, especially for the control
metformin 14166 results of Chang et al. did not support a cardiovascular protective effect of acarbose compared to metformin in Taiwan populations [[57]].A series of recent clinical trials clarified the relationship between acarbose
Select Disease Character Offset Disease Term Instance
diabetes mellitus 419 ChinaPublication date (collection): /2018Publication date (epub): 5/2018AbstractMetabolic diseases, especially diabetes mellitus , have become global health issues. The etiology of diabetes mellitus can be attributed to genetic and/or
diabetes mellitus 488 5/2018AbstractMetabolic diseases, especially diabetes mellitus, have become global health issues. The etiology of diabetes mellitus can be attributed to genetic and/or environmental factors. Current evidence suggests the association
diabetes mellitus 1405 agents. In conclusion, gut microbiota may provide a novel viewpoint for the treatment of patients with diabetes mellitus .1. IntroductionOver the past few decades, metabolic diseases such as type 2 diabetes mellitus (T2DM),
diabetes mellitus 1499 with diabetes mellitus.1. IntroductionOver the past few decades, metabolic diseases such as type 2 diabetes mellitus (T2DM), obesity, dyslipidemia, and cardiovascular diseases have become major public health issues all
diabetes mellitus 3755 [[15]–[17]]. All this information suggests that gut microbiota may be involved in the etiology of diabetes mellitus .Short-chain fatty acids (SCFAs) including acetate (C2), propionate (C3), butyrate (C4), and valerate
diabetes mellitus 4376 in diabetic rats [[22]]. Thus, SCFAs might have a promising role in the prevention and treatment of diabetes mellitus .Currently available therapeutic options for T2DM, especially glucose-lowering agents, target different
diabetes mellitus 5174 microbiota (Table 1) to better understand the role of the intestinal microenvironment in the treatment of diabetes mellitus .2. Metformin and Gut Microbiota2.1. Metformin Mechanism of Action and Side EffectsMetformin is a biguanide
diabetes mellitus 15750 glucose responses to carbohydrates in vivo. As mentioned previously, SCFAs play an important role in diabetes mellitus . Acarbose was found to increase serum butyrate levels in individuals with impaired glucose tolerance.
diabetes mellitus 16237 production of acetate and propionate is significantly decreased [[26]].The beneficial effects of acarbose on diabetes mellitus , such as reduction of inflammatory cytokines and regulation of SCFA levels, can be related to the alteration
diabetes mellitus 20635 of great significance for understanding the role of gut microbiota as novel therapeutic targets in diabetes mellitus . However, further studies are still needed to confirm the hypothesis.6. ConclusionIn conclusion, the
diabetes mellitus 22405 [[68]]SitagliptinRoseburia [[13]]Bifdobacterium [[13]]Blautia [[13]]HF/HC-STZ SD rats [[13]]T2DM: type 2 diabetes mellitus ; HFD: high-fat diet; PPAR-γ: peroxisome proliferator-activated receptor γ; DPP-4: dipeptidyl peptidase-4;
hyperglycemia 1872 such diseases. One of the most common metabolic disorders is T2DM, which is characterized by chronic hyperglycemia that can be attributed to genetic and/or environmental factors. Recently, the role played by gut microbiota
hyperglycemia 12945 oligosaccharides into mono- and disaccharides in the intestinal lumen [[29]]. The control of postprandial hyperglycemia is especially important in Asia due to the traditional carbohydrate-rich dietary pattern [[49]]. In
hyperglycemia 13391 Therefore, acarbose is an effective and safe antidiabetic agent, especially for the control of postprandial hyperglycemia . The major cause of acarbose side effects (e.g., diarrhea, flatulence, and abdominal distention) is
hypoglycemia 17726 glucagon levels, slow gastric emptying, accelerate satiety, induce weight loss, and lower the risk of hypoglycemia [[29]]. Grasset et al. [[65]] demonstrated that GLP-1 sensitivity was modulated by gut microbiota through
metabolic syndrome 19011 medicine Danshensu Bingpian Zhi (DBZ), a PPAR-γ partial agonist, not only improved the phenotypes of metabolic syndrome but also increased the Bacteroidetes/Firmicutes ratio, resulting in an increase in Akkermansia muciniphila
obesity 1525 IntroductionOver the past few decades, metabolic diseases such as type 2 diabetes mellitus (T2DM), obesity , dyslipidemia, and cardiovascular diseases have become major public health issues all over the world.
obesity 9267 metformin on intestinal microbiota. The abundance of Akkermansia muciniphila was found to be decreased in obesity and diabetes [[9]], while higher baseline levels were associated with improvements in the cardiometabolic
obesity 9395 while higher baseline levels were associated with improvements in the cardiometabolic parameters of obesity [[11], [42]]. Experimental studies revealed that the abundances of Akkermansia muciniphila [[43], [44]]
type 2 diabetes mellitus 1492 patients with diabetes mellitus.1. IntroductionOver the past few decades, metabolic diseases such as type 2 diabetes mellitus (T2DM), obesity, dyslipidemia, and cardiovascular diseases have become major public health issues all
type 2 diabetes mellitus 22398 rats [[68]]SitagliptinRoseburia [[13]]Bifdobacterium [[13]]Blautia [[13]]HF/HC-STZ SD rats [[13]]T2DM: type 2 diabetes mellitus ; HFD: high-fat diet; PPAR-γ: peroxisome proliferator-activated receptor γ; DPP-4: dipeptidyl peptidase-4;

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