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©The Author(s) 2022. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Jun 7, 2022; 28(21): 2320-2333
Published online Jun 7, 2022. doi: 10.3748/wjg.v28.i21.2320
Published online Jun 7, 2022. doi: 10.3748/wjg.v28.i21.2320
Intermittent hypoxia is involved in gut microbial dysbiosis in type 2 diabetes mellitus and obstructive sleep apnea-hypopnea syndrome
Sha-Sha Tang, Cheng-Hong Liang, Ya-Lei Liu, Wei Wei, Xin-Ru Deng, Xiao-Yang Shi, Li-Min Wang, Li-Jun Zhang, Hui-Juan Yuan, Department of Endocrinology, Henan Provincial Key Medicine Laboratory of Intestinal Microecology and Diabetes, Henan Provincial People’s Hospital, People’s Hospital of Zhengzhou University, Zhengzhou 450003, Henan Province, China
Author contributions: Tang SS designed the research and conducted microbiome analysis; Liu YL conducted the research except the microbiome analysis; Tang SS and Liang CH analyzed the microbiome data and wrote the paper; all other data were analyzed by Shi XY and Deng XR with oversight by Wei W; Zhang LJ and Wang LM were responsible for the data acquisition and input and proofreading of the manuscript; Tang SS and Yuan HJ had primary responsibility for the final content; all authors have read and approved the final manuscript.
Supported by National Natural Science Foundation of China , No. 81970705 ; and Central Plains Thousand Talents Plan , No. 204200510026 .
Institutional review board statement: This study was reviewed and approved by the Ethics Committee of Henan Provincial People’s Hospital (IRB No. 2019-62).
Informed consent statement: All study participants provided informed written consent before the study enrollment.
Conflict-of-interest statement: All authors declare no conflicts of interest.
Data sharing statement: Raw sequencing data and associated metadata were deposited in the NCBI short-read archive with BioProject accession number PRJNA788301.
STROBE statement: The authors have read the STROBE Statement—checklist of items, and the manuscript was prepared and revised according to the STROBE Statement—checklist of items.
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: https://creativecommons.org/Licenses/by-nc/4.0/
Corresponding author: Hui-Juan Yuan, PhD, Chief Doctor, Department of Endocrinology, Henan Provincial Key Medicine Laboratory of Intestinal Microecology and Diabetes, Henan Provincial People’s Hospital, People’s Hospital of Zhengzhou University, No. 7 Weiwu Road, Zhengzhou 450003, Henan Province, China. hjyuan@zzu.edu.cn
Received: January 8, 2022
Peer-review started: January 8, 2022
First decision: March 9, 2022
Revised: March 19, 2022
Accepted: April 22, 2022
Article in press: April 22, 2022
Published online: June 7, 2022
Processing time: 145 Days and 8.7 Hours
Peer-review started: January 8, 2022
First decision: March 9, 2022
Revised: March 19, 2022
Accepted: April 22, 2022
Article in press: April 22, 2022
Published online: June 7, 2022
Processing time: 145 Days and 8.7 Hours
Core Tip
Core Tip: Clinically, type 2 diabetes mellitus (T2DM) patients have a significantly higher prevalence of obstructive sleep apnea-hypopnea syndrome (OSAHS) than non-T2DM patients and are more prone to diabetes-related complications and metabolic syndrome, including obesity and hypertension. In recent years, the imbalance of gut microbiota has been found to be associated with various metabolic disorders. This study revealed that intermittent hypoxia was associated with changes in the gut microbiota in patients with T2DM complicated by OSAHS. These changes may be involved in the progression of metabolic disorders through increased proinflammatory factors and impaired intestinal barrier function.