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妊娠期糖尿病合并体重过度增加会加剧新生儿肠道微生物群失调,这与 、 和 的丰度降低有关。

Gestational diabetes-combined excess weight gain exacerbates gut microbiota dysbiosis in newborns, associated with reduced abundance of , , and .

作者信息

Xiao Yunshan, Shi Yuan, Ni Yan, Ni Meilan, Yang Yuxin, Zhang Xueqin

机构信息

Department of Obstetrics, Women and Children's Hospital, School of Medicine, Xiamen University, Xiamen, China.

Xiamen Key Laboratory of Basic and Clinical Research on Major Obstetrical Diseases, Women and Children's Hospital, School of Medicine, Xiamen University, Xiamen, China.

出版信息

Front Cell Infect Microbiol. 2024 Dec 13;14:1496447. doi: 10.3389/fcimb.2024.1496447. eCollection 2024.

DOI:10.3389/fcimb.2024.1496447
PMID:39726807
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11670820/
Abstract

BACKGROUND

Existing literature indicates that Gestational diabetes mellitus (GDM) and maternal obesity disrupt the normal colonization of the neonatal gut microbiota alone. Still, the combined impact of GDM and excessive gestational weight gain (EGWG) on this process remains under explored. The association between gestational weight gain before/after GDM diagnosis and neonatal gut microbiota characteristics is also unclear.The purpose of this study is to conduct investigation and analysis on the above-mentioned issues, providing a basis for optimizing clinical management plans.

METHODS

This study involved 98 mother-infant pairs categorized into GDM and non-GDM groups. The GDM group was further subdivided based on gestational weight gain (GWG) into normal (GDM+NGWG) and excessive (GDM+EGWG) weight gain groups. Neonatal stool samples were collected within 24 hours post-delivery for gut microbiota profiling through 16S rRNA gene sequencing. Statistical analyses explored correlations between total GWG/BMI gain and those before/after GDM diagnosis (t-GWG/GBG; b-GWG/GBG; a-GWG/GBG) with key bacterial taxa.

RESULTS

Notable genus-level changes included enrichment of and , and depletion of , , , among GDM-Total and GDM+EGWG groups compared to non-GDM. Further,LEfSe analysis identified 30 differential bacteria taxa between GDM-Total and healthy control groups, which increased to 38 between GDM+EGWG and non-GDM groups, highlighting more pronounced microbial shifts associated with EGWG. was negatively correlated with t-GWG and newborn birth weight; The showed a negative correlation with t-GWG, t-GBG, and a-GBG. Additionally, exhibited negative correlations with t-GBG and a-GBG.

CONCLUSION

This study has identified that the presence of EGWG in GDM mothers further exacerbated neonatal gut microbial perturbations. Total GWG/GBG and those after the diagnosis of GDM were negatively correlated with the abundance of neonatal gut , , and . These findings provide new insights for precise prevention and management of GDM.

摘要

背景

现有文献表明,妊娠期糖尿病(GDM)和孕妇肥胖各自都会破坏新生儿肠道微生物群的正常定植。然而,GDM与孕期体重过度增加(EGWG)对这一过程的综合影响仍有待探索。GDM诊断前后的孕期体重增加与新生儿肠道微生物群特征之间的关联也不明确。本研究的目的是对上述问题进行调查和分析,为优化临床管理方案提供依据。

方法

本研究纳入了98对母婴,分为GDM组和非GDM组。GDM组根据孕期体重增加(GWG)进一步细分为正常(GDM+NGWG)和过度(GDM+EGWG)体重增加组。在分娩后24小时内收集新生儿粪便样本,通过16S rRNA基因测序进行肠道微生物群分析。统计分析探讨了总GWG/BMI增加量与GDM诊断前后(t-GWG/GBG;b-GWG/GBG;a-GWG/GBG)与关键细菌类群之间的相关性。

结果

与非GDM组相比,GDM-总组和GDM+EGWG组在属水平上有显著变化,包括[具体菌属1]和[具体菌属2]的富集,以及[具体菌属3]、[具体菌属4]、[具体菌属5]、[具体菌属6]的减少。此外,线性判别分析效应大小(LEfSe)分析确定GDM-总组与健康对照组之间有30种差异细菌类群,GDM+EGWG组与非GDM组之间增加到38种,突出了与EGWG相关的更明显的微生物变化。[具体菌属7]与t-GWG和新生儿出生体重呈负相关;[具体菌属8]与t-GWG、t-GBG和a-GBG呈负相关。此外,[具体菌属9]与t-GBG和a-GBG呈负相关。

结论

本研究发现GDM母亲中EGWG的存在进一步加剧了新生儿肠道微生物的紊乱。总GWG/GBG以及GDM诊断后的增加量与新生儿肠道[具体菌属7]、[具体菌属8]和[具体菌属9]的丰度呈负相关。这些发现为GDM的精准预防和管理提供了新的见解。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9b5f/11670820/b341508bc116/fcimb-14-1496447-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9b5f/11670820/1c910b2adb9a/fcimb-14-1496447-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9b5f/11670820/19fde2ecaa72/fcimb-14-1496447-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9b5f/11670820/1cfcb9478044/fcimb-14-1496447-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9b5f/11670820/23fcc8d8d1da/fcimb-14-1496447-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9b5f/11670820/61bbd3fa5779/fcimb-14-1496447-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9b5f/11670820/b341508bc116/fcimb-14-1496447-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9b5f/11670820/1c910b2adb9a/fcimb-14-1496447-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9b5f/11670820/19fde2ecaa72/fcimb-14-1496447-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9b5f/11670820/1cfcb9478044/fcimb-14-1496447-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9b5f/11670820/23fcc8d8d1da/fcimb-14-1496447-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9b5f/11670820/61bbd3fa5779/fcimb-14-1496447-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9b5f/11670820/b341508bc116/fcimb-14-1496447-g006.jpg

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