The final, formatted version of the article will be published soon.
ORIGINAL RESEARCH article
Front. Microbiol.
Sec. Microbial Physiology and Metabolism
Volume 15 - 2024 |
doi: 10.3389/fmicb.2024.1473441
Suppression of certain intestinal microbiota metabolites may lead to gestational diabetes in mice fed a high-fat diet
Provisionally accepted- 1 The Second Affiliated Hospital of Fujian Medical University, Quanzhou, China
- 2 Fujian Medical University, Fuzhou, Fujian Province, China
Abstract Background: We aim to establish a gestational diabetes mellitus (GDM) mouse model with mice fed with a high-fat diet (HFD) in comparison with pregnant mice with normal blood glucose levels to investigate the role of intestinal microbiota in the development of HFD-induced GDM. Methods: We divided healthy 6-week-old female C57BL mice into an HFD-induced GDM group and a normal diet group. Their bacterial flora and metabolites in intestinal fecal exosomes were co-analysed using 16s multi-region sequencing and compared. Findings: Alpha (α) diversity was lower within the model group compared to the control group. Beta (β) diversity was significantly different between the two groups. The relative abundances of Lactobacillus, Actinomyces, Rothia, and Bacteroidetes were significantly different between the two groups. Fermentation and nitrate consumption were significantly higher in the GDM group. Multiple bacteria were associated with glycerophosphocholine, S-methyl-5′-thioadenosine, quinolinate, galactinol, deoxyadenosine, DL-arginine, and 2-oxoadenic acid. Interpretation: Imbalances in the production of Lactobacillus, Bacteroidetes, Actinomyces, and Rothia and their related metabolites may lead to metabolic disturbances in GDM. These indicators may be used to assess changes affecting the intestinal microbiota during pregnancy and thus help modulate diet and alter blood glucose.
Keywords: gestational diabetes mellitus, intestinal microbiota, Exosomes, high-fat diet, short-chain fatty acids deoxyadenosine, dl-arginine, and 2-oxoadenic acid
Received: 31 Jul 2024; Accepted: 02 Sep 2024.
Copyright: © 2024 Xie, Zhao, Lin, Wang, Liu and Xie. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence:
Baoyuan Xie, The Second Affiliated Hospital of Fujian Medical University, Quanzhou, China
Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.