Variation of Carbohydrate-Active Enzyme Patterns in the Gut Microbiota of Italian Healthy Subjects and Type 2 Diabetes Patients

GLP-1 stimulates insulin secretion, suppresses glucagon secretion, delays gastric emptying, and inhibits small bowel motility, all actions contributing to the anti-diabetogenic peptide effect. Endothelial dysfunction is strongly associated with insulin resistance and type 2 diabetes mellitus and may cause the angiopathy typifying this debilitating disease. Therefore, interventions affecting both endothelial dysfunction and insulin resistance may prove useful in improving survival in type 2 diabetes patients. We investigated GLP-1's effect on endothelial function and insulin sensitivity (SI) in two groups: 1) 12 type 2 diabetes patients with stable coronary artery disease and 2) 10 healthy subjects with normal endothelial function and SI. Subjects underwent infusion of recombinant GLP-1 or saline in a random crossover study. Endothelial function was measured by postischemic FMD of brachial artery, using ultrasonography. SI [in (10−4 dl·kg−1·min−1)/(μU/ml)] was measured by hyperinsulinemic isoglycemic clamp technique. In type 2 diabetic subjects, GLP-1 infusion significantly increased relative changes in brachial artery diameter from baseline FMD(%) (3.1 ± 0.6 vs. 6.6 ± 1.0%, P < 0.05), with no significant effects on SI (4.5 ± 0.8 vs. 5.2 ± 0.9, P = NS). In healthy subjects, GLP-1 infusion affected neither FMD(%) (11.9 ± 0.9 vs. 10.3 ± 1.0%, P = NS) nor SI (14.8 ± 1.8 vs. 11.6 ± 2.0, P = NS). We conclude that GLP-1 improves endothelial dysfunction but not insulin resistance in type 2 diabetic patients with coronary heart disease. This beneficial vascular effect of GLP-1 adds yet another salutary property of the peptide useful in diabetes treatment.

Download Full-text

Galacto-oligosaccharides ameliorate dysbiotic Bifidobacteriaceae decline in Japanese patients with type 2 diabetes

Beneficial Microbes ◽

10.3920/bm2016.0230 ◽

2017 ◽

Vol 8 (5) ◽

pp. 705-716 ◽

Cited By ~ 12

Author(s):

M. Gonai ◽

A. Shigehisa ◽

I. Kigawa ◽

K. Kurasaki ◽

O. Chonan ◽

...

Keyword(s):

Type 2 Diabetes ◽

Glucose Tolerance ◽

Gut Microbiota ◽

Impaired Glucose Tolerance ◽

Healthy Subjects ◽

Metabolic Diseases ◽

Healthy Individuals ◽

Patients With Diabetes ◽

Metabolic Endotoxemia

Gut microbiota affects the host’s metabolism, and it is suggested that there are differences in gut microbiota composition between patients with type 2 diabetes and healthy individuals. Additionally, dysbiosis may increase the concentration of lipopolysaccharides (LPS), causing metabolic endotoxemia, which induces impaired glucose tolerance. Several studies have reported relationships between metabolic diseases and the gut microbiota; and prebiotics, such as oligosaccharides, are commonly consumed to regulate gut microbiotas in healthy individuals. Galacto-oligosaccharides (GOS) are a major prebiotic, which specifically increase Bifidobacteriaceae abundance. Recent studies have reported that Bifidobacteriaceae improved metabolic endotoxemia or impaired glucose tolerance. However, there are few studies reporting the effects of GOS on patients with type 2 diabetes. In the current study, we compared clinical parameters, faecal gut microbiota, their associated metabolic products and their components such as LPS, and LPS-binding protein (LBP) produced by the host, between patients with diabetes and healthy controls. We then assessed the effects of GOS on glycaemic control, and gut microbiotas and metabolites in patients with type 2 diabetes in a double-blind controlled manner. LBP levels were significantly higher in patients with diabetes than those of healthy subjects, which was consistent with previous reports. The abundance of Bifidobacteriaceae and the diversity of intestinal microbiota were significantly lower in patients with diabetes than in healthy subjects. Interestingly, Bifidobacteriaceae was markedly restored in patients with diabetes after consumption of GOS, whereas LBP and glucose tolerance did not improve during this short-term trial period. In the present study, we demonstrated that GOS can ameliorate dysbiosis in patients with diabetes, and continuous intake of GOS may be a promising method for managing type 2 diabetes.

Download Full-text

The Effect on Gut Microbiota Structure of Primarily Diagnosed Type 2 Diabetes Patients Intervened by Sancai Lianmei Particle and Acarbose: A Randomized Controlled Trial

Journal of Clinical Trials ◽

10.4172/2167-0870.1000270 ◽

2016 ◽

Vol 6 (3) ◽

Cited By ~ 3

Author(s):

Wei Fang ◽

Chenchen Wei

Keyword(s):

Type 2 Diabetes ◽

Randomized Controlled Trial ◽

Gut Microbiota ◽

Controlled Trial ◽

Randomized Controlled ◽

Microbiota Structure ◽

Diabetes Patients

Download Full-text

Population pharmacokinetics of carvedilol enantiomers and their metabolites in healthy subjects and type-2 diabetes patients

European Journal of Pharmaceutical Sciences ◽

10.1016/j.ejps.2017.05.033 ◽

2017 ◽

Vol 109 ◽

pp. S108-S115 ◽

Cited By ~ 4

Author(s):

Glauco H.B. Nardotto ◽

Vera L. Lanchote ◽

Eduardo B. Coelho ◽

Oscar Della Pasqua

Keyword(s):

Type 2 Diabetes ◽

Population Pharmacokinetics ◽

Healthy Subjects ◽

Diabetes Patients

Download Full-text

Measurement of GLP-1 in Impaired Glucose Tolerance Subjects in Comparison to Type 2 Diabetes Patients and Healthy Subjects

International Journal of Biology ◽

10.5539/ijb.v5n4p29 ◽

2013 ◽

Vol 5 (4) ◽

Cited By ~ 1

Author(s):

Ahmed Abdullah Ebeid ◽

Mohammad Hosam El- deen Zaghloul ◽

Mahmoud Abdulhakam Darwish ◽

Ossama A. Mansour

Keyword(s):

Type 2 Diabetes ◽

Glucose Tolerance ◽

Impaired Glucose Tolerance ◽

Healthy Subjects ◽

Diabetes Patients

Download Full-text

Influence of CYP2C19 genotype on the pharmacokinetics of R483, a CYP2C19 substrate, in healthy subjects and type 2 diabetes patients

European Journal of Clinical Pharmacology ◽

10.1007/s00228-010-0840-3 ◽

2010 ◽

Vol 66 (10) ◽

pp. 1005-1015 ◽

Cited By ~ 8

Author(s):

Katrijn Bogman ◽

Mariabeth Silkey ◽

Siew Pheng Chan ◽

Brian Tomlinson ◽

Cornelia Weber

Keyword(s):

Type 2 Diabetes ◽

Healthy Subjects ◽

Cyp2c19 Genotype ◽

Diabetes Patients

Download Full-text

Alteration of Gut Microbiota in type 2 Diabetes Complicated with Cholelithiasis Patients

10.21203/rs.3.rs-52504/v1 ◽

2020 ◽

Author(s):

Jiajia Chen ◽

Linlin Yan ◽

Xingfan Ma ◽

Ping Yuan ◽

Fan Zhao ◽

...

Keyword(s):

Type 2 Diabetes ◽

Gut Microbiota ◽

Elevated Serum ◽

Serum Triglyceride ◽

16S Rrna Gene Sequencing ◽

Epidemiological Studies ◽

Rrna Gene ◽

Microbial Composition ◽

Diabetes Patients

Abstract Background: Epidemiological studies showed that diabetes patients are more prone to developing cholelithiasis. Although composition of gut microbiota in type 2 diabetes or cholelithiasis have been studied respectively, the underlying role of gut microbiota in developing from diabetes to cholelithiasis remains unclear. By 16S rRNA gene sequencing, the gut microbial composition of 33 healthy subjects, 53 type 2 diabetes, 31 cholelithiasis and 32 type 2 diabetes complicated with cholelithiasis patients were studied. Results: Microbial diversity significantly decreased in type 2 diabetes complicated with cholelithiasis patients. In type 2 diabetes patients, phylum Proteobacteria class Gammaproteobacteria and order Lactobacillales were significantly increased. In cholelithiasis patients, phylum Bacteroidetes, class Bacteroidia order Bacteroidales family Bacteroidaceae and genus Bacteroides were significantly increased. There were also significant increases of phylum Proteobacteria, class Gammaproteobacteria order Lactobacillales family Lactobacillaceae and genus Lactobacillus in type 2 diabetes complicated with cholelithiasis patients accompanied by elevated serum triglyceride and total bile acids. Conclusions: The results show similar but more intricate gut microbiota dysbiosis in type 2 diabetes complicated with cholelithiasis compared with type 2 diabetes, which might partially explain the mechanism of type 2 diabetes as the risk factor of cholelithiasis from the perspective of gut microbiota.

Download Full-text