Identification of therapeutic effect of glucagon‐like peptide 1 in the treatment of STZ‐induced diabetes mellitus in rats by restoring the balance of intestinal flora

Yuan, Xiao; Ni, Haixiang; Chen, Xialiang; Feng, Xing; Wu, Qiaomin; Chen, Jie

doi:10.1002/jcb.27343

Cited by 20 publications

(22 citation statements)

References 35 publications

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“…However, it is still controversial whether GLP-1 receptors are present on OTU_98 OTU_56 OTU_196 OTU_12 OTU_68 OTU_122 OTU_10 OTU_59 OTU_96 OTU_17 OTU_35 OTU_46 OTU_78 OTU_92 OTU_119 OTU_170 HFD1 HFD2 HFD3 HFD4 HFD5 HFD6 HFD7 HFD8 NC1 NC2 NC3 NC4 NC5 NC6 NC7 human hepatocytes [26,27]. Recent studies have reported that GLP-1 prevents diabetes by altering the structure of the gut microbiota and inhibiting inflammation [28,29]. Inflammation, caused by a high-fat diet, is one factor inducing metabolic disorders [30].…”

Section: Discussionmentioning

confidence: 99%

“…Increased Firmicutes/Bacteroidetes ratio results in decreased SCFA production and increased energy harvested from the diet, facilitating the development and progression of NAFLD [5]. Some studies have reported that a higher Firmicutes/Bacteroidetes ratio was decreased by liraglutide in obese and diabetic rats [17,28,29]. However, the relationship of Firmicutes/Bacteroidetes ratio with obesity and NAFLD remains controversial [37][38][39].…”

Section: Discussionmentioning

confidence: 99%

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Liraglutide Attenuates Nonalcoholic Fatty Liver Disease by Modulating Gut Microbiota in Rats Administered a High-Fat Diet

Zhang

Tao

Gao

et al. 2020

BioMed Research International

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This study aimed to determine whether modulation of the gut microbiota structure by liraglutide helps improve nonalcoholic fatty liver disease (NAFLD) in rats on a high-fat diet (HFD). Rats were administered an HFD for 12 weeks to induce NAFLD and then administered liraglutide for 4 additional weeks. Next-generation sequencing and multivariate analysis were performed to assess structural changes in the gut microbiota. Liraglutide attenuated excessive hepatic ectopic fat deposition, maintained intestinal barrier integrity, and alleviated metabolic endotoxemia in HFD rats. Liraglutide significantly altered the overall structure of the HFD-disrupted gut microbiota and gut microbial composition in HFD rats in comparison to those on a normal diet. An abundance of 100 operational taxonomic units (OTUs) were altered upon liraglutide administration, with 78 OTUs associated with weight gain or inflammation. Twenty-three OTUs positively correlated with hepatic steatosis-related parameters were decreased upon liraglutide intervention, while 5 OTUs negatively correlated with hepatic steatosis-related parameters were increased. These results suggest that liraglutide-mediated attenuation of NAFLD partly results from structural changes in gut microbiota associated with hepatic steatosis.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Liraglutide Attenuates Nonalcoholic Fatty Liver Disease by Modulating Gut Microbiota in Rats Administered a High-Fat Diet

Zhang

Tao

Gao

et al. 2020

BioMed Research International

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“…The damage of the intestinal barrier function leads to an increase in permeability and an increase in the level of in ammatory factors such as LPS in the blood circulation. Some studies have done HE staining on the ileal tissue of mice in the diabetic state, and observed severe destruction of the intestinal mucosa [30]. Clostridium butyricum can accelerate the growth of intestinal mucosal epithelial cells and promote intestinal peristalsis.…”

Section: Discussionmentioning

confidence: 99%

Correlation study on gut microbiota and omentin-1 gene polymorphism in Uyghur newly diagnosed type 2 diabetes

Nuli

Shan

Zhang

et al. 2020

Preprint

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Background: Type 2 diabetes (T2DM) is a top risk factor for health in China. Gut microbiota, genetic factors and lipids metabolism play important role in development of T2DM. In this study, we investigated the relationship between the gut microbiota and omentin-1 gene polymorphism to explore the interaction between host gene and gut microbiota in Uyghur T2DM. Methods: A total of 98 newly diagnosed Uyghur T2DM patients and 99 healthy normal controls (NC) enrolled into this study according to inclusion criteria. The total DNAs was extracted from the fecal microbiota. Abundance of the Lactobacillus genus, Bacteroides thetaiotaomicron and Clostridium in the gut microbiota was determined with 16S rDNA gene Real-time fluorescence quantitative PCR amplification. PCR-PFLP was applied to determine the genotypes of Val109Asp variant (rs2274907) in the Omentin-1 gene. And the relationship between rs2274907 and gut microbiota was assessed. Results: There were no significant differences of the Val109Asp variant (rs2274907) between T2DM and NC group. The abundance of Lactobacillus genus and Clostridium genus was lower in newly diagnosed T2DM group than in the NC group (P<0.05). Serum insulin, LDL-C, the abundances of Lactobacillus genus and Clostridium genus were the risk factors of T2DM. (OR=1.094 95%CI 1.014-1.180), (OR=3.868 95%CI 1.250-11.971), (OR=0.288 95%CI 0.145-0.571), (OR=0.044 95%CI 0.012-0.154). Conclusions: The abundance of Lactobacillus and Clostridium genus may be related to the pathogenesis of new-onset T2DM in Uyghur population, the mechanism of which needs to be further studied. The interactive relationship between the gut microbiota and omentin-1 gene polymorphism in newly diagnosed T2DM was not observed in this study.

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“…For example, recently it was reported that a rhubarb extract, Rhein, increasing the intestinal population of Bacteroidetes, mediates an increase in ileal GLP-1 producing cells, peripheral GLP-1(7-36) NH2 levels and improved glucose tolerance in diabetic db/db mice ( 395 ). Consistently, STZ-treated rats, are protected from oxidative and inflammatory stress when treated with Liraglutide, and Bacteroides , as well as Lactobacilli strain populations appear to be restored ( 396 ).…”

Section: The Microbiotamentioning

confidence: 93%

Dissecting the Physiology and Pathophysiology of Glucagon-Like Peptide-1

Paternoster

Falasca

2018

Front. Endocrinol.

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An aging world population exposed to a sedentary life style is currently plagued by chronic metabolic diseases, such as type-2 diabetes, that are spreading worldwide at an unprecedented rate. One of the most promising pharmacological approaches for the management of type 2 diabetes takes advantage of the peptide hormone glucagon-like peptide-1 (GLP-1) under the form of protease resistant mimetics, and DPP-IV inhibitors. Despite the improved quality of life, long-term treatments with these new classes of drugs are riddled with serious and life-threatening side-effects, with no overall cure of the disease. New evidence is shedding more light over the complex physiology of GLP-1 in health and metabolic diseases. Herein, we discuss the most recent advancements in the biology of gut receptors known to induce the secretion of GLP-1, to bridge the multiple gaps into our understanding of its physiology and pathology.

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Identification of therapeutic effect of glucagon‐like peptide 1 in the treatment of STZ‐induced diabetes mellitus in rats by restoring the balance of intestinal flora

Abstract: In summary, the findings of this study confirmed the antihyperglycemic effect of GLP-1 and demonstrated that the therapeutic effect of GLP-1 in the treatment of STZ-induced DM was mediated, at least partially, by its ability to restore the balance of intestinal flora.

Cited by 20 publications

References 35 publications

Liraglutide Attenuates Nonalcoholic Fatty Liver Disease by Modulating Gut Microbiota in Rats Administered a High-Fat Diet

Liraglutide Attenuates Nonalcoholic Fatty Liver Disease by Modulating Gut Microbiota in Rats Administered a High-Fat Diet

Correlation study on gut microbiota and omentin-1 gene polymorphism in Uyghur newly diagnosed type 2 diabetes

Dissecting the Physiology and Pathophysiology of Glucagon-Like Peptide-1

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