Investigation of gut microbiome changes in type 1 diabetic mellitus rats based on high-throughput sequencing

Ma, Quantao; Li, Yaqi; Wang, Jingkang; Li, Pengfei; Duan, Yuhui; Dai, Hongyu; An, Yongcheng; Cheng, Lijun; Wang, Tieshan; Wang, Chunguo; Wang, Ting; Zhao, Baosheng

doi:10.1016/j.biopha.2020.109873

Cited by 107 publications

(66 citation statements)

References 63 publications

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“…Among them, Candidatus Arthromitus plays a key role in mouse intestinal immune function control and its downregulation may be associated with intestinal inflammatory imbalance [49]. In addition, AGE-D mice showed a decrease of a butyrate-producing bacterial genus, Anaerostipes, that is inversely related to inflammation and insulin resistance, since butyrate is reported as one of the most important short-chain fatty acids (SCFAs) in the maintenance of colonic health [50]. Moreover, we also found an increase of Parabacteroides, Ruminococcus (Lachnospiraceae family) and Lawsonia in the AGE-D group.…”

Section: Discussionmentioning

confidence: 99%

“…Moreover, we also found an increase of Parabacteroides, Ruminococcus (Lachnospiraceae family) and Lawsonia in the AGE-D group. An abnormal increase in Lachnospiraceae has been recently proposed as one of the factors involved in metabolic diseases such as diabetes and obesity [50], but the mechanism through which these bacteria affect these conditions is still unclear. It has been proposed that members of Lachnospiraceae may be involved in intestinal lipopolysaccharide translocation in blood, thus becoming one of the causes of the inflammatory processes which characterize these metabolic diseases [51].…”

Section: Discussionmentioning

confidence: 99%

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Effects of Exogenous Dietary Advanced Glycation End Products on the Cross-Talk Mechanisms Linking Microbiota to Metabolic Inflammation

et al. 2020

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Heat-processed diets contain high amounts of advanced glycation end products (AGEs). Here we explore the impact of an AGE-enriched diet on markers of metabolic and inflammatory disorders as well as on gut microbiota composition and plasma proteins glycosylation pattern. C57BL/6 mice were allocated into control diet (CD, n = 15) and AGE-enriched diet (AGE-D, n = 15) for 22 weeks. AGE-D was prepared replacing casein by methylglyoxal hydroimidazolone-modified casein. AGE-D evoked increased insulin and a significant reduction of GIP/GLP-1 incretins and ghrelin plasma levels, altered glucose tolerance, and impaired insulin signaling transduction in the skeletal muscle. Moreover, AGE-D modified the systemic glycosylation profile, as analyzed by lectin microarray, and increased Nε-carboxymethyllysine immunoreactivity and AGEs receptor levels in ileum and submandibular glands. These effects were associated to increased systemic levels of cytokines and impaired gut microbial composition and homeostasis. Significant correlations were recorded between changes in bacterial population and in incretins and inflammatory markers levels. Overall, our data indicates that chronic exposure to dietary AGEs lead to a significant unbalance in incretins axis, markers of metabolic inflammation, and a reshape of both the intestinal microbiota and plasma protein glycosylation profile, suggesting intriguing pathological mechanisms underlying AGEs-induced metabolic derangements.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Effects of Exogenous Dietary Advanced Glycation End Products on the Cross-Talk Mechanisms Linking Microbiota to Metabolic Inflammation

et al. 2020

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“…In comparison with radiation-free mice here, TAI exposure downregulated butyrate levels, a member of SCFAs, which was further decreased in fecal pellets of mice subjected to P80 challenge. Since Allobaculum is thought to be a beneficial bacterium, which plays anti-inflammatory role, protects gut barrier function and regulates host metabolism and immunity by producing SCFAs in the intestine (Cox et al, 2014;Ma et al, 2020). Thus, P80-treated mice may harbor lower relative abundance of Allobaculum in the intestinal microbiota.…”

Section: Discussionmentioning

confidence: 99%

Gut Microbiota Metabolite Fights Against Dietary Polysorbate 80-Aggravated Radiation Enteritis

Xiao

Dong

et al. 2020

Front. Microbiol.

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Radiation therapy is a cornerstone of modern management methods for malignancies but is accompanied by diverse side effects. In the present study, we showed that food additives such as polysorbate 80 (P80) exacerbate irradiation-induced gastrointestinal (GI) tract toxicity. A 16S ribosomal RNA high-throughput sequencing analysis indicated that P80 consumption altered the abundance and composition of the gut microbiota, leading to severe radiation-induced GI tract injury. Mice harboring fecal microbes from P80-treated mice were highly susceptible to irradiation, and antibiotics-challenged mice also represented more sensitive to radiation following P80 treatment. Importantly, butyrate, a major metabolite of enteric microbial fermentation of dietary fibers, exhibited beneficial effects against P80 consumption-aggravated intestinal toxicity via the activation of G-protein-coupled receptors (GPCRs) and maintenance of the intestinal bacterial composition in irradiated animals. Moreover, butyrate had broad therapeutic effects on common radiation-induced injury. Collectively, our findings demonstrate that P80 are potential risk factors for cancer patients during radiotherapy and indicate that butyrate might be employed as a therapeutic option to mitigate the complications associated with radiotherapy.

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“…Zhang et al reported that the family Bacteroidaceae was dysregulated in a diabetic mouse model [38]. Previous studies have shown that the abundance levels of Lactobacillus and Allobaculum, bene cial bacteria that can directly protect intestinal barrier function, are reduced in diabetic animal models [39,40].…”

Section: Discussionmentioning

confidence: 99%

Pyridostigmine Protects Against Diabetic Cardiomyopathy by Regulating Gut Microbiota and Branched-Chain Amino Acid Catabolism to Attenuate Mitochondria Dysfunction

Yang

Zhao

et al. 2020

Preprint

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Background: Recent studies have reported that disruption of gut microbes and their metabolites is associated with diabetic cardiomyopathy, but the mechanism by which gut microbes improve diabetic cardiomyopathy remains unclear. Method: Male C57BL/6J mice with high-fat diet and streptozotocin-induced diabetic cardiomyopathy were studied in comparison with control littermates. Diabetic mice were either untreated or subjected to daily intragastric of pyridostigmine. After 10 weeks of hyperglycaemia, vagus activity, cardiac function and cardiac structure were measured by heart rate variability assessment, echocardiography, and immunohistochemistry. The intestinal barrier and gut microbiota were evaluated by fluorescence in situ hybridization and high-throughput sequencing. Additionally, plasma and cardiac branched-chain amino acid (BCAA) distribution and cardiac BCAA catabolism were determined. The structure and respiratory function of mitochondria were measured to assess cardiac mitochondria performance. Results: Intestinal permeability and tight junctions were impaired, bacterial translocation was increased, vagal activity was decreased in mice with diabetic cardiomyopathy mice. Additionally, gut microbes in mice with diabetic cardiomyopathy were disrupted, especially key microbes related to diabetes and BCAA production. Pyridostigmine, which reversibly inhibits cholinesterase to improve autonomic imbalance, enhanced vagus nerve activity, improved insulin resistance and cardiac damage, and alleviated intestinal barrier injury and gut microbiota disruption. Specifically, pyridostigmine decreased the abundance of diabetes-non-protective microbes and increased that of diabetes-protective microbes and BCAA-producing microbes. Pyridostigmine decreased cardiac BCAA concentrations by impairing gut microbe-mediated BCAA production. Furthermore, pyridostigmine upregulated BCAT2 and PP2Cm expression and decreased P-BCKDHA/BCKDHA and BCKDK expression, thus improving cardiac BCAA catabolism. Interestingly, the mitochondrial structural and functional disruption in mice with diabetic cardiomyopathy was attenuated after pyridostigmine administration, which may indicate one of the mechanisms by which BCAAs reduce cardiac damage. Conclusions: In conclusion, intestinal barrier, gut microbiota and vagal activity were impaired in mice with diabetic cardiomyopathy. Pyridostigmine ameliorated insulin resistance and cardiomyopathy, with an effect related to regulated gut microbes and its metabolite BCAA catabolism to attenuate mitochondria dysfunction of heart. These results provide novel insights for the development of a therapeutic strategy for diabetes-induced cardiac damage that targets gut microbes and BCAA catabolism.

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Investigation of gut microbiome changes in type 1 diabetic mellitus rats based on high-throughput sequencing

Cited by 107 publications

References 63 publications

Effects of Exogenous Dietary Advanced Glycation End Products on the Cross-Talk Mechanisms Linking Microbiota to Metabolic Inflammation

Effects of Exogenous Dietary Advanced Glycation End Products on the Cross-Talk Mechanisms Linking Microbiota to Metabolic Inflammation

Gut Microbiota Metabolite Fights Against Dietary Polysorbate 80-Aggravated Radiation Enteritis

Pyridostigmine Protects Against Diabetic Cardiomyopathy by Regulating Gut Microbiota and Branched-Chain Amino Acid Catabolism to Attenuate Mitochondria Dysfunction

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