Dietary fibre, gut microbiota dysbiosis and type 2 diabetes

Background: The prevalence of type 2 diabetes is on the increase globally and it represents about 90% of adults who are diagnosed with diabetes. Overweight and obesity, lifestyle, genetic predisposition and gut microbiota dysbiosis have been implicated as possible risk factors in the development of type 2 diabetes. In particular, low intake of dietary fibres and consumption of foods high in fat and sugar which are common in western lifestyle have been reported to contribute to the depletion of specific bacterial taxa. Therefore, it is possible that the intake of dietary fibre may alter the environment in the gut and provide the needed substrate for microbial bloom. Aim: The current review is a systematic review and meta-analysis which evaluates the role of dietary fibre in modulating gut microbiota dysbiosis in patients with type 2 diabetes. Methods: This is a systematic review and meta-analysis of randomised controlled trials which relied on the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) framework. Electronic searches were conducted using EBSCOHost with links to Health Sciences Research Databases (encompassing Academic Search Premier, MEDLINE, Psychology and Behavioral Sciences Collection, APA PsycInfo, CINAHL Plus with Full Text and APA PsycArticles databases), EMBASE and Google Scholar. The reference lists of articles were also searched for relevant studies. Searches were conducted from date of commencement of database to 5^th August, 2020. The search strategy was based on the Populations, Intervention, Comparator, Outcomes, Studies (PICOS) framework and involved the use of synonyms and medical subject headings (MesH). Search terms were combined with Boolean operators (OR/AND). Results: Nine studies which met the inclusion criteria were selected for the systematic review and meta-analysis and four distinct areas were identified: The effect of dietary fibre on gut microbiota; The role of dietary fibre on short chain fatty acids (SCFAs); Glycaemic control and Adverse events. There was significant difference (P<0.01) in the relative abundance of bifidobacterium with a mean difference of 0.72 (95% CI, 0.56, 0.89) between the dietary fibre group compared with placebo. In relation to the meta-analysis for SCFAs, while there was significant difference (P=0.02) between the dietary fibre group and placebo with a standardised mean difference of 0.5 (95% CI, 0.08, 0.91) regarding total SCFAs, the differences were not significant (P>0.05) in relation to acetic acid, propionic acid and butyric acid. There was only significant improvement (P=0.002) with respect to glycated haemoglobin with a mean difference of -0.18 (95% CI, -0.29, -0.06) between the dietary fibre group and placebo group. Differences between the two groups were not significant (P>0.05) in relation to fasting blood glucose and Homeostatic Model Assessment of Insulin Resistance (HOMAR – IR). Furthermore, there were no significant differences between the two groups in subjects who reported adverse events. It is possible that the promotion of SCFA producers in greater diversity and abundance by dietary fibre in this review led to improvement in glycated haemoglobin, partly due to increased glucagon-like peptide-1 (GLP – 1) production. In addition, Bifidobacterium lactis has been reported to increase glycogen synthesis, decrease expression of hepatic gluconeogenesis – genes, improve translocation of glucose transport– 4 and promote glucose uptake. It is also possible that the reduction in body weight of participants in the intervention group compared with control may have contributed to the observed improvement in glycated haemoglobin. Conclusion: This systematic review and meta-analysis have demonstrated that dietary fibre can significantly improve (P<0.05) the relative abundance of bifidobacterium, total SCFAs and glycated haemoglobin. However, dietary fibre did not appear to have significant effect (P>0.05) on fasting blood glucose, HOMAR – IR, acetic acid, propionic acid, butyric acid and adverse events.