The Second School of Clinical Medicine, Southern Medical University, Guangzhou, 510515, People's Republic of China.
Department of Geriatric Endocrinology, Guangdong Provincial Geriatrics Institute (East Zone), Guangdong Academy of Medical Sciences, Guangdong Provincial People's Hospital, No. 3, Chanchugang, Zhongshan 2nd Road, Yuexiu District, Guangzhou, 510080, Guangdong Province, People's Republic of China.
Mol Med. 2023 Sep 8;29(1):122. doi: 10.1186/s10020-023-00716-4.
Children of mothers with gestational diabetes mellitus (GDM) are more prone to acquire type 2 diabetes and obesity as adults. Due to this link, early intervention strategies that alter the gut microbiome may benefit the mother and kid long-term. This work uses metagenomic and transcriptome sequencing to investigate how probiotics affect gut microbiota dysbiosis and inflammation in GDM.
GDM and control metagenomic sequencing data were obtained from the SRA database. This metagenomic data helped us understand gut microbiota abundance and function. KEGG detected and extracted functional pathway genes. Transcriptome sequencing data evaluated GDM-related gene expression. Finally, GDM animal models were given probiotics orally to evaluate inflammatory response, regulatory immune cell fractions, and leptin protein levels.
GDM patients had more Fusobacteria and Firmicutes, while healthy people had more Bacteroidetes. Gut microbiota composition may affect GDM by altering the L-aspartate and L-asparagine super pathways. Mannan degradation and the super pathway of L-aspartate and L-asparagine synthesis enhanced in GDM mice with leptin protein overexpression. Oral probiotics prevent GDM by lowering leptin. Oral probiotics increased Treg, Tfr, and Breg cells, which decreased TNF-α and IL-6 and increased TGF-β and IL-10, preventing inflammation and preserving mouse pregnancy.
Dysbiosis of the gut microbiota may increase leptin expression and cause GDM. Oral probiotics enhance Treg, Tfr, and Breg cells, which limit the inflammatory response and assist mice in sustaining normal pregnancy. Thus, oral probiotics may prevent GDM, enabling targeted gut microbiota modulation and maternal and fetal health.
患有妊娠糖尿病（GDM）的母亲所生的孩子成年后更容易患上 2 型糖尿病和肥胖症。由于这种联系，改变肠道微生物组的早期干预策略可能对母亲和孩子的长期健康有益。本研究采用宏基因组和转录组测序技术，研究益生菌如何影响 GDM 患者的肠道微生物失调和炎症。
从 SRA 数据库中获取 GDM 和对照组的宏基因组测序数据。这些宏基因组数据有助于我们了解肠道微生物群的丰度和功能。KEGG 检测和提取功能途径基因。转录组测序数据评估 GDM 相关基因表达。最后，通过口服给予 GDM 动物模型益生菌，评估炎症反应、调节性免疫细胞亚群和瘦素蛋白水平。
GDM 患者的 Fusobacteria 和 Firmicutes 丰度较高，而健康人的 Bacteroidetes 丰度较高。肠道微生物群组成可能通过改变 L-天冬氨酸和 L-天冬酰胺超级途径来影响 GDM。GDM 小鼠中 leptin 蛋白过表达，甘露聚糖降解和 L-天冬氨酸和 L-天冬酰胺合成的超级途径增强。口服益生菌通过降低瘦素来预防 GDM。口服益生菌增加了 Treg、Tfr 和 Breg 细胞，降低了 TNF-α和 IL-6，增加了 TGF-β和 IL-10，从而防止了炎症并维持了小鼠妊娠。
肠道微生物群失调可能会增加瘦素的表达，导致 GDM。口服益生菌增强了 Treg、Tfr 和 Breg 细胞，从而限制了炎症反应，帮助小鼠维持正常妊娠。因此，口服益生菌可能预防 GDM，实现针对肠道微生物群的调节和母婴健康。
