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Review
.2020 Jul 15;11(7):293-308.
doi: 10.4239/wjd.v11.i7.293.

Gut microbiota and diabetes: From correlation to causality and mechanism

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Review

Gut microbiota and diabetes: From correlation to causality and mechanism

Wei-Zheng Li et al. World J Diabetes..

Abstract

In this review, we summarize the recent microbiome studies related to diabetes disease and discuss the key findings that show the early emerging potential causal roles for diabetes. On a global scale, diabetes causes a significant negative impact to the health status of human populations. This review covers type 1 diabetes and type 2 diabetes. We examine promising studies which lead to a better understanding of the potential mechanism of microbiota in diabetes diseases. It appears that the human oral and gut microbiota are deeply interdigitated with diabetes. It is that simple. Recent studies of the human microbiome are capturing the attention of scientists and healthcare practitioners worldwide by focusing on the interplay of gut microbiome and diabetes. These studies focus on the role and the potential impact of intestinal microflora in diabetes. We paint a clear picture of how strongly microbes are linked and associated, both positively and negatively, with the fundamental and essential parts of diabetes in humans. The microflora seems to have an endless capacity to impact and transform diabetes. We conclude that there is clear and growing evidence of a close relationship between the microbiota and diabetes and this is worthy of future investments and research efforts.

Keywords: Causality; Diabetes; Inflammation; Insulin resistance; Mechanism; Metabolites; Microbiota; Type 1 diabetes; Type 2 diabetes.

©The Author(s) 2020. Published by Baishideng Publishing Group Inc. All rights reserved.

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Conflict of interest statement

Conflict-of-interest statement: The authors declare no conflicts of interest for this article.

Figures

Figure 1
Figure 1
The main mechanism of gut microbiota affecting insulin resistance and diabetes. Gut microbes are influenced by diet, genetics and medication, and common types of interventions in humans include fecal microbiota transplantation, metformin and probiotics. Lipopolysaccharide (LPS), short-chain fatty acids (SCFAs) and bile acids are major regulators of diabetes. LPS binds to the Toll-like receptor 4 to induce low-grade inflammation and insulin resistance. Bile acids are synthesized by the liver and transformed into secondary bile acids through the metabolism of gut microbiota. Secondary bile acids activate Farnesoid X receptor to induce increased secretion of fibroblast growth factor 15/19. Secondary bile acids activate Takeda G protein-coupled receptor to stimulate intestinal L cells to secrete glucagon-like peptide-1 (GLP-1). SCFAs activate L cells to promote the release of GLP-1 and peptide YY to increase insulin sensitivity. SCFAs also have a regulatory effect on T cells. LPS: Lipopolysaccharide; TLR4: Toll-like receptor 4; FXR: Farnesoid X receptor; FGF15/19: Fibroblast growth factor 15/19; TGR5: Takeda G protein-coupled receptor 5; PYY: Peptide YY; GLP-1: Glucagon-like peptide-1; SCFAs: Short-chain fatty acids; FFAR 2: Free fatty acid receptor 2; FFAR 3: Free fatty acid receptor 3; FMT: Fecal microbiota transplantation.
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References

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