Obesity and diabetes are growing global health concern, as the number of adults living with diabetes globally has more than quadrupled since 1980 (1). In the U.S., 11.3% of the population are living with type 2 diabetes, and many more with prediabetes (2). Impaired glucose homeostasis and metabolic dysregulation are key features of obesity and type 2 diabetes, and gut hormones, microbiota, and microRNAs are critical mediators of this process. Although genetics certainly has a role to play in this process, there is a growing recognition of the role that the environment and holobiont (host plus commensal microbes), and its associated hologenome, contribute to host physiology and disease outcomes (3–5). In this Research Topic, we explore the interplay between gut hormones, microRNAs, and microbiota in glucose homeostasis, and how perturbations to these systems lead to metabolic dysregulation.
Specifically, here, Farhat et al. review microbiome changes that occur in women with gestational diabetes mellitus and their offspring, while Liu S. et al. investigate the interaction of the microbiome and testosterone levels in men with type 2 diabetes. Although reproducibility in microbiome research is challenging due to the considerable variability in extraction, library preparation, sequencing, and analysis pipelines, the increasing application of meta-transcriptomics will aid in identifying functional convergences that will be of critical value in informing disease progression and treatment.
Additionally, Liu C. et al. discuss mechanisms of GLP-1-mediated regulation of glucose homeostasis, including circadian rhythm and its disruption. The microbiome is no exception to circadian rhythms, and Liu C. et al. explore some of these intersecting pathways and report on their impact on GLP-1 secretion. Finally, Palihaderu et al. provide insight into the role that microRNAs - RNAs that negatively regulate the target gene expression either by degradation or translational repression of targeted mRNAs – play in insulin resistance. Importantly, both microRNAs and gut hormones are implicated in abnormal glucose homeostasis in obesity and diabetes and are emerging as important targets to treat diabetes-associated complications.
We are optimistic that future directions of these research areas will include bench-to-bedside applications to target enteroendocrine factors or miRNAs to treat diabetes.
Statements
Author contributions
RG: Writing – review & editing. LM: Writing – original draft. RRG: Writing – review & editing. XS: Writing – review & editing.
Conflict of interest
The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
Publisher’s note
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.
References
1
Available at: https://www.who.int/news-room/fact-sheets/detail/diabetes.
2
3
TurnbaughPJLeyREHamadyMFraser-LiggettCMKnightRGordonJ. The human microbiome project. Nature (2007) 449:804–10. doi: 10.1038/nature06244
4
PostlerTSGhoshS. Understanding the holobiont: how microbial metabolites affect human health and shape the immune system. Cell Metab (2017) 26(1):110–30. doi: 10.1016/j.cmet.2017.05.008
5
Summary
Keywords
gut hormones, microbiota, miRNAs, obesity and type 2 diabetes, glucose homeostasis, metabolism
Citation
Matz LM, Geesala R, Gaddam RR and Shi X-Z (2023) Editorial: Understanding the role of gut hormones, microbiota, and miRNAs in metabolic regulation and glucose homeostasis in obesity and type-2-diabetes. Front. Endocrinol. 14:1255942. doi: 10.3389/fendo.2023.1255942
Received
10 July 2023
Accepted
21 July 2023
Published
18 August 2023
Volume
14 - 2023
Edited and reviewed by
Jeff M. P. Holly, University of Bristol, United Kingdom
Updates
Copyright
© 2023 Matz, Geesala, Gaddam and Shi.
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) and the copyright owner(s) 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: Ramasatyaveni Geesala, rageesal@utmb.edu
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.