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Analysis of gut microbiota of obese individuals with type 2 diabetes and healthy individuals.

ABSTRACT: Type 2 diabetes mellitus (T2DM) accounts for 90% of diabetes cases worldwide. The majority of T2DM patients are obese. Dysbiosis in the gut microflora is strongly associated with the pathogenesis of obesity and T2DM; however, the microbiome of obese-T2DM individuals in the Pakistani population remains unexplored. The gut microbiota signature of 60 Pakistani adults was studied using 16S rRNA sequencing targeting V3-V4 hypervariable regions. The sequence analysis revealed that bacteria from Firmicutes were predominant along with those from Clostridia and Negativicutes, whereas bacteria from Verrucomicrobia, Bacteroidetes, Proteobacteria, and Elusimicrobia were less abundant among the obese T2DM patients. These data distinctively vary from those in reports on the Indian population. The difference in gut microbiota could presumably be related to the distinct lifestyle and eastern dietary habits (high carbohydrate and fat intake, low fiber intake) and unregulated antibiotic consumption. This is the first study carried out to understand the gut microbiome and its correlation with individual life style of obese T2DM patients in the Pakistani population.

SUBMITTER: Ahmad A

PROVIDER: S-EPMC6938335 | biostudies-literature | 2019

REPOSITORIES: biostudies-literature

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Analysis of gut microbiota of obese individuals with type 2 diabetes and healthy individuals.

Ahmad Aftab A Yang Wanwei W Chen Guofang G Shafiq Muhammad M Javed Sundus S Ali Zaidi Syed Shujaat SS Shahid Ramla R Liu Chao C Bokhari Habib H

PloS one 20191231 12

Type 2 diabetes mellitus (T2DM) accounts for 90% of diabetes cases worldwide. The majority of T2DM patients are obese. Dysbiosis in the gut microflora is strongly associated with the pathogenesis of obesity and T2DM; however, the microbiome of obese-T2DM individuals in the Pakistani population remains unexplored. The gut microbiota signature of 60 Pakistani adults was studied using 16S rRNA sequencing targeting V3-V4 hypervariable regions. The sequence analysis revealed that bacteria from Firmic ...[more]

PMID: 31891582

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Project description:BackgroundInteractions between the diet and intestinal microbiota play a role in health and disease, including obesity and related metabolic complications. There is great interest to use dietary means to manipulate the microbiota to promote health. Currently, the impact of dietary change on the microbiota and the host metabolism is poorly predictable and highly individual. We propose that the responsiveness of the gut microbiota may depend on its composition, and associate with metabolic changes in the host.MethodologyOur study involved three independent cohorts of obese adults (n = 78) from Belgium, Finland, and Britain, participating in different dietary interventions aiming to improve metabolic health. We used a phylogenetic microarray for comprehensive fecal microbiota analysis at baseline and after the intervention. Blood cholesterol, insulin and inflammation markers were analyzed as indicators of host response. The data were divided into four training set - test set pairs; each intervention acted both as a part of a training set and as an independent test set. We used linear models to predict the responsiveness of the microbiota and the host, and logistic regression to predict responder vs. non-responder status, or increase vs. decrease of the health parameters.Principal findingsOur models, based on the abundance of several, mainly Firmicute species at baseline, predicted the responsiveness of the microbiota (AUC = 0.77-1; predicted vs. observed correlation = 0.67-0.88). Many of the predictive taxa showed a non-linear relationship with the responsiveness. The microbiota response associated with the change in serum cholesterol levels with an AUC of 0.96, highlighting the involvement of the intestinal microbiota in metabolic health.ConclusionThis proof-of-principle study introduces the first potential microbial biomarkers for dietary responsiveness in obese individuals with impaired metabolic health, and reveals the potential of microbiota signatures for personalized nutrition.

Project description:Dietary supplementation with complex carbohydrates is known to alter the composition of gut microbiota, and optimal implementation of the use of these so called "prebiotics" could be of great potential in prevention and possibly treatment of obesity and associated cardiometabolic and inflammatory diseases via changes in the gut microbiota. An alternative to this "microbiocentric view" is the idea that health-promoting effects of certain complex carbohydrates reside in the host, and could secondarily affect the diversity and abundance of gut microbiota. To circumvent this potential interpretational problem, we aimed at providing an overview about whether and how dietary supplementation of different complex carbohydrates changes the gut microbiome in healthy non-obese individuals. We then reviewed whether the reported changes in gut bacterial members found to be established by complex carbohydrates would benefit or harm the cardiometabolic and immunological health of the host taking into account the alterations in the microbiome composition and abundance known to be associated with obesity and its associated disorders. By combining these research areas, we aimed to give a better insight into the potential of (foods containing) complex carbohydrates in the treatment and prevention of above-mentioned diseases. We conclude that supplemental complex carbohydrates that increase Bifidobacteria and Lactobacilli, without increasing the deleterious Bacteroides, are most likely promoting cardiometabolic and immunological health in obese subjects. Because certain complex carbohydrates also affect the host's immunity directly, it is likely that host-microbiome interactions in determination of health and disease characteristics are indeed bidirectional. Overall, this review article shows that whereas it is relatively clear in which direction supplemental fermentable carbohydrates can alter the gut microbiome, the relevance of these changes regarding health remains controversial. Future research should take into account the different causes of obesity and its adverse health conditions, which in turn have drastic effects on the microbiome balance.

Project description:Intestinal homeostasis underpins the development of type 1 diabetes (T1D), and dietary manipulations to enhance intestinal homeostasis have been proposed to prevent T1D. The current study aimed to investigate the efficacy of supplementing a novel specific low-methoxyl pectin (LMP) dietary fiber in preventing T1D development. Female NOD mice were weaned onto control or 5% (wt/wt) LMP supplemented diets for up to 40 weeks of age, overt diabetes incidence and blood glucose were monitored. Then broad-spectrum antibiotics (ABX) treatment per os for 7 days followed by gut microbiota transfer was performed to demonstrate gut microbiota-dependent effects. Next-generation sequencing was used for analyzing the composition of microbiota in caecum. Concentration of short chain fatty acids were determined by GC-MS. The barrier reinforcing tight junction proteins zonula occludens-2 (ZO-2), claudin-1 and NOD like receptor protein 3 (NLRP3) inflammasome activation were determined by Western blot. The proportion of CD25+Foxp3+CD4+ regulatory T cell (Foxp3+ Treg) in the pancreas, pancreatic and mesenteric lymph nodes was analyzed by flow cytometry. We found that LMP supplementation ameliorated T1D development in non-obese diabetic (NOD) mice, as evidenced by decreasing diabetes incidence and fasting glucose levels in LMP fed NOD mice. Further microbiota analysis revealed that LMP supplementation prevented T1D-associated caecal dysbiosis and selectively enriched caecal bacterial species to produce more SCFAs. The LMP-mediated microbial balance further enhanced caecal barrier function and shaped gut-pancreatic immune environment, as characterized by higher expression of tight junction proteins claudin-1, ZO-2 in caecum, increased Foxp3+ Treg population and decreased NLRP3 inflammasome activation in both caecum and pancreas. The microbiota-dependent beneficial effect of LMP on T1D was further proven by the fact that aberration of caecal microbiota by ABX treatment worsened T1D autoimmunity and could be restored with transfer of feces of LMP-fed NOD mice. These data demonstrate that this novel LMP limits T1D development by inducing caecal homeostasis to shape pancreatic immune environment. This finding opens a realistic option for gut microbiota manipulation and prevention of T1D in humans.

Dataset Information

Analysis of gut microbiota of obese individuals with type 2 diabetes and healthy individuals.

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Analysis of gut microbiota of obese individuals with type 2 diabetes and healthy individuals.

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