Editorial: Relationship between gestational and neonatal diabetes mellitus

Bukhari, Ihtisham; Iqbal, Furhan; Thorne, Rick F.

doi:10.3389/fendo.2022.1060147

Cited by 3 publications

(2 citation statements)

References 6 publications

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“…A growing number of studies suggest that dysregulated gut microbiota increases adiposity, β-cell dysfunction, metabolic endotoxemia, systemic inflammation, and oxidative stress, ultimately driving the development of T2DM (Galicia-Garcia et al 2020 ; Fang et al 2022 ; Zhou et al 2022 ). Furthermore, the question of whether gestational diabetes mellitus (GDM) can result in neonatal diabetes mellitus (NDM) or postpartum diabetes is of significant importance (Bukhari et al 2022a , b ). The higher relative abundance of Prevotellaceae was associated with obesity and impaired glucose metabolism (Zheng et al 2021 ).…”

Section: Discussionmentioning

confidence: 99%

Oral probiotics increased the proportion of Treg, Tfr, and Breg cells to inhibit the inflammatory response and impede gestational diabetes mellitus

Liang,

Feng,

Yang

et al. 2023

Mol Med

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Background 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. Methods 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. Results 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. Conclusion 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.

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Section: Discussionmentioning

confidence: 99%

Oral probiotics increased the proportion of Treg, Tfr, and Breg cells to inhibit the inflammatory response and impede gestational diabetes mellitus

Liang,

Feng,

Yang

et al. 2023

Mol Med

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“…Gestational diabetes mellitus (GDM), characterized by increased peripheral insulin resistance (IR), may cause fetal complications, including weight gain, glucose intolerance, and death. However, its effect on NDM remains uncertain [9].…”

Section: Introductionmentioning

confidence: 99%

Exploring the Diet-Gut Microbiota-Epigenetics Crosstalk Relevant to Neonatal Diabetes

Alsharairi

2023

Genes

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Neonatal diabetes (NDM) is a rare monogenic disorder that presents as hyperglycemia during the first six months of life. The link between early-life gut microbiota dysbiosis and susceptibility to NDM remains uncertain. Experimental studies have demonstrated that gestational diabetes mellitus (GDM) could develop into meconium/gut microbiota dysbiosis in newborns, and thus, it is thought to be a mediator in the pathogenesis of NDM. Epigenetic modifications have been considered as potential mechanisms by which the gut microbiota and susceptibility genes interact with the neonatal immune system. Several epigenome-wide association studies have revealed that GDM is associated with neonatal cord blood and/or placental DNA methylation alterations. However, the mechanisms linking diet in GDM with gut microbiota alterations, which may in turn induce the expression of genes linked to NDM, are yet to be unraveled. Therefore, the focus of this review is to highlight the impacts of diet, gut microbiota, and epigenetic crosstalk on altered gene expression in NDM.

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G protein-coupled receptor 1 participating in the mechanism of mediating gestational diabetes mellitus by phosphorylating the AKT pathway

Zhu,

Huang,

Chai

et al. 2024

Open Life Sciences

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Gestational diabetes mellitus (GDM) is a metabolic disease that occurs during pregnancy. Herein, we investigate G protein-coupled receptor 1 (GPR1) in mediating GDM through the phosphorylation of serine/threonine kinase (AKT) pathway. Thirty pregnant SD rats were grouped into: normal pregnancy control group (NC), GDM model group, and GDM model + high-dose GPR1 antagonist treatment (GDM + Ari) group. GDM model was established, and the GDM + Ari group adopted GPR1 antagonist aripiprazole. The blood glucose level, insulin level, and insulin resistance (IR) were detected. The expression and phosphorylation of GPR1, AKT, and extracellular signal-regulated kinase (ERK) in placental tissue were detected using reverse transcription-polymerase chain reaction (RT-PCR) and western blotting (WB). The serum insulin concentration, glucose concentration, and glycated hemoglobin concentration during pregnancy in GDM group SD rats were significantly higher than those in the NC group (P < 0.05). The expression and phosphorylation levels of GPR1, AKT, and ERK in the placental tissue of SD pregnant rats in the GDM group were significantly lower than those in the NC group. Furthermore, compared with the GDM group, the expression of GPR1, AKT, and ERK in placental tissue was significantly reduced in the GDM + Ari group, while simultaneously enhancing the blood glucose level and IR level. In addition, the survival number, body weight, and malformation rate of the offspring of the GDM + Ari group were significantly improved, and there was no significant effect on the number of offspring. The expressions of GPR1, AKT, and ERK in placental tissue exhibited a significant decrease, while the glucose level and IR were observed to increase in the GDM + Ari group. Enhancing the expression of GPR1 may activate AKT phosphorylation to alleviate GDM. GPR1 could potentially serve as a novel target for diabetes treatment, offering new insights into managing GDM.

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Editorial: Relationship between gestational and neonatal diabetes mellitus

Cited by 3 publications

References 6 publications

Oral probiotics increased the proportion of Treg, Tfr, and Breg cells to inhibit the inflammatory response and impede gestational diabetes mellitus

Oral probiotics increased the proportion of Treg, Tfr, and Breg cells to inhibit the inflammatory response and impede gestational diabetes mellitus

Exploring the Diet-Gut Microbiota-Epigenetics Crosstalk Relevant to Neonatal Diabetes

G protein-coupled receptor 1 participating in the mechanism of mediating gestational diabetes mellitus by phosphorylating the AKT pathway

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