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Insights into the gut microbiota of Nigerian elderly with type 2 diabetes and non-diabetic elderly persons.

ABSTRACT: Type 2 diabetes (T2D) is a prevalent non-communicable disease among the world's growing elderly population. The contribution of the gut microbiota to T2D in several Westernized countries has been established. However, there is little information on the role of the gut microbiota in T2D from the African continent where lifestyle and life expectancy are different. Aims:This study sought to investigate gut microbiota variation in relation to elderly people living with T2D. in Nigeria. Methods:Whole microbial community DNA were derived from the stool samples of healthy urban-dwelling elderly individuals and urban-dwelling elderly individuals with T2D. The V4 region of the 16S rRNA gene was Illumina-sequenced and analyzed using QIIME2. Results:Beta taxonomic diversity was significantly different between healthy elderly individuals and elderly individuals with T2D. However, no difference in the alpha taxonomic diversity and predicted functional alpha diversity of the gut microbiota was observed. The genus Ruminococcus (T2D versus Healthy: 2.89% vs 2.21%), families Coriobacteriaceae (Collinsella, T2D versus Healthy: 2.62 % vs 1.25%) and Bifidobacteriaceae were enriched in elderly individuals with T2D, while members of Clostridiaceae (Clostridium, Healthy versus T2D: 5.6% vs 3.2%) and Peptostreptococcaceae (Healthy versus T2D: 3.45% vs 1.99%) were enriched in healthy volunteers. Pathways involved in amino acid biosynthesis were enriched in elderly individuals with T2D, while pathways involved in respiration and the biosynthesis of vital building blocks were enriched in healthy volunteers. Conclusions:The study demonstrated for the first time in an African elderly population that the abundance of Bifidobacteriaceae, Collinsella, and Ruminococcus within the gut varies in relation to T2D. Findings from this study suggest that the restoration of features associated with healthiness via the way of gut microbiota modification could be one step needed to improve elderly patient care.

SUBMITTER: Afolayan AO

PROVIDER: S-EPMC7262409 | biostudies-literature | 2020 May

REPOSITORIES: biostudies-literature

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Insights into the gut microbiota of Nigerian elderly with type 2 diabetes and non-diabetic elderly persons.

Afolayan A O AO Adebusoye L A LA Cadmus E O EO Ayeni F A FA

Heliyon 20200529 5

Type 2 diabetes (T2D) is a prevalent non-communicable disease among the world's growing elderly population. The contribution of the gut microbiota to T2D in several Westernized countries has been established. However, there is little information on the role of the gut microbiota in T2D from the African continent where lifestyle and life expectancy are different.<h4>Aims</h4>This study sought to investigate gut microbiota variation in relation to elderly people living with T2D. in Nigeria.<h4>Met ...[more]

PMID: 32490229

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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.

Project description:The incidence of type 1 diabetes (T1D) is determined by both genetic and environmental factors. In recent years, the gut microbiota have been identified to be an important environmental factor that could modify diabetes susceptibility. We have previously shown that Myeloid differentiation primary response gene 88 (MyD88), a major adaptor protein downstream of most innate immune Toll-like receptor (TLR) signaling, is important for mediating diabetes susceptibility in the non-obese diabetic (NOD) mouse model of human T1D. Here we report the role of TIR-domain-containing adapter-inducing interferon-β (TRIF) in T1D development, as TRIF is an important adaptor protein downstream of TLR3 and TLR4 signaling. We found that TRIF-deficient (TRIF-/-) NOD mice were protected from development of diabetes, but only when housed with TRIF-deficient (TRIF-/-) NOD mice. When housed with TRIF-sufficient wild type (WT, i.e., TRIF+/+) NOD mice, the mice developed diabetes. We further investigated the gut microbiota as a potential cause for the altered diabetes development. Interestingly, TRIF-/-NOD mice had a different microbiota composition compared to WT NOD mice, only if they were housed with TRIF-/-NOD mice. However, the composition of gut microbiota in the TRIF-/-NOD mice was indistinguishable from WT NOD mice, if they were housed with WT NOD mice. The difference in the gut microbiota in TRIF-/-NOD mice, due to cohousing, accorded with the diabetes development in TRIF-/-NOD mice. Comparing the gut microbiota in TRIF-/- and WT NOD mice, we identified changes in percentage of Sutterella, Rikenella and Turicibacter species. Moreover, bacteria from WT NOD mice induced significantly stronger inflammatory immune responses in vitro compared to those from TRIF-/-NOD mice. Further immunological analysis revealed impaired function of dendritic cells and reduced T cell activation and proliferation in TRIF-/-NOD mice. Our data show that TRIF-deficiency protects NOD mice from diabetes development through alteration of the gut microbiota and reduced immune cell activation; however, that protection is over-ridden upon exposure to WT NOD bacteria. Therefore exposure to different microbiota can modify disease susceptibility determined by genetic factors related to innate immunity.

Dataset Information

Insights into the gut microbiota of Nigerian elderly with type 2 diabetes and non-diabetic elderly persons.

Publications

Insights into the gut microbiota of Nigerian elderly with type 2 diabetes and non-diabetic elderly persons.

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