Review
Copyright ©The Author(s) 2021. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Diabetes. Aug 15, 2021; 12(8): 1146-1163
Published online Aug 15, 2021. doi: 10.4239/wjd.v12.i8.1146
Gut microbiota as a target for prevention and treatment of type 2 diabetes: Mechanisms and dietary natural products
Fan Xia, Lu-Ping Wen, Bing-Chen Ge, Yu-Xin Li, Fang-Ping Li, Ben-Jie Zhou
Fan Xia, Lu-Ping Wen, Bing-Chen Ge, Ben-Jie Zhou, Department of Pharmacy, The Seventh Affiliated Hospital of Sun Yat-Sen University, Shenzhen 518107, Guangdong Province, China
Yu-Xin Li, Department of Pharmacology, Guangdong Medical University, Zhanjiang 524023, Guangdong Province, China
Fang-Ping Li, Department of Endocrinology, The Seventh Affiliated Hospital, Sun Yat-Sen University, Shenzhen 518107, Guangdong Province, China
Author contributions: Xia F contributed to the literature review and analysis, and drafted the paper; Wen LP, Li FP, and Zhou BJ contributed equally to the paper in conception and critical revision and editing; all authors approved the final version.
Supported by National Natural Science Foundation of China, No. 81803816 and No. 82074078.
Conflict-of-interest statement: The authors have nothing to disclose.
Open-Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/Licenses/by-nc/4.0/
Corresponding author: Ben-Jie Zhou, PhD, Chief Pharmacist, Postdoc, Professor, Department of Pharmacy, The Seventh Affiliated Hospital of Sun Yat-Sen University, No. 628 Zhenyuan Road, Guangming District, Shenzhen 518107, Guangdong Province, China. zhoubj163@163.com
Received: January 28, 2021
Peer-review started: January 29, 2021
First decision: May 3, 2021
Revised: May 10, 2021
Accepted: July 5, 2021
Article in press: July 5, 2021
Published online: August 15, 2021
Abstract

Type 2 diabetes mellitus (T2DM) is among the most remarkable public health concerns globally. Accumulating research evidence documents that alteration of gut microbiota has an indispensable role in the onset and progression of obesity and T2DM. A reduced microbial diversity is linked to insulin resistance and energy metabolism, especially for the rise of the Firmicutes/Bacteroidetes ratio. Changes in metabolites followed by the gut dysbacteriosis are linked to the presence of T2DM. Moreover, endotoxin leakage and gut permeability caused by gut dysbacteriosis is more of a trigger for the onset and progression of T2DM. Research documents that natural products are remarkable arsenals of bioactive agents for the discovery of anti-T2DM drugs. Many studies have elucidated that the possible mechanisms of the anti-T2DM effects of natural products are remarkably linked to its regulation on the composition of gut microflora and the successive changes in metabolites directly or indirectly. This review presents a brief overview of the gut microbiota in T2DM and several relevant mechanisms, including short-chain fatty acids, biosynthesis and metabolism of branched-chain fatty acids, trimethylamine N-oxide, bile acid signaling, endotoxin leakage, and gut permeability, and describes how dietary natural products can improve T2DM via the gut microbiota.

Keywords: Diabetes, Obesity, Gut microbiota, Mechanisms, Dietary natural products, Metabolites

Core Tip: Numerous natural products possessing prebiotic effects like fruits, vegetables, and medicinal plants, have been found to ameliorate type 2 diabetes mellitus by modulating gut microbiota composition and abundance, reducing the gut permeability, and subsequently increasing the production of short-chain fatty acids and biosynthesis and metabolism of branched-chain fatty acids, decreasing the level of lipopolysaccharide, and inhibiting the inflammation.