ReviewInternational journal of molecular sciences2022
Epigenetic Links between Microbiota and Gestational Diabetes.
Review in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
11 citing papers in PubMed, 35 citations in OpenAlex.
- Microbiome alterations in healthy pregnancy and pregnancy disorders in association with autoimmune diseases.Folia microbiologica · 2026Review
- Article
- Reduced maternal SCFAs in GDM diminish GPR43 signaling and induce offspring CAKUT.Communications biology · 2025Article
- Deciphering DNA Methylation in Gestational Diabetes Mellitus: Epigenetic Regulation and Potential Clinical Applications.International journal of molecular sciences · 2024Review
- Interactions between host and gut microbiota in gestational diabetes mellitus and their impacts on offspring.BMC microbiology · 2024Review
- Dynamic changes in the gut microbiota during three consecutive trimesters of pregnancy and their correlation with abnormal glucose and lipid metabolism.European journal of medical research · 2024Article
- G protein-coupled receptor 1 participating in the mechanism of mediating gestational diabetes mellitus by phosphorylating the AKT pathway.Open life sciences · 2024Article
- Gestational diabetes mellitus: Impacts on fetal neurodevelopment, gut dysbiosis, and the promise of precision medicine.Frontiers in molecular biosciences · 2024Review
- Gestational diabetes-combined excess weight gain exacerbates gut microbiota dysbiosis in newborns, associated with reduced abundance ofFrontiers in cellular and infection microbiology · 2024Article
- Oral probiotics increased the proportion of Treg, Tfr, and Breg cells to inhibit the inflammatory response and impede gestational diabetes mellitus.Molecular medicine (Cambridge, Mass.) · 2023Article
- Microbiome Changes in Pregnancy Disorders.Antioxidants (Basel, Switzerland) · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Gestational diabetes mellitus (GDM) is considered a significant and increasing worldwide problem. The growing body of evidence on this topic has allowed us to point out that a hostile intrauterine environment in mothers with GDM via epigenetic mechanisms induces "diabetogenic" and "obesogenic" changes in an offspring's DNA. This sets a vicious intergenerational cycle of metabolic diseases in motion, gradually deteriorating the health of the human population. One of the most important participants of this process seems to be altered microbiota. There is a chance that the identification of specific epigenetic marks may provide a key for future diagnostic, prognostic and therapeutic solutions in the field of personalised medicine. Given the reversibility of most epigenetic changes, there is an opportunity to improve the long-term health of the human population. In this manuscript, we aim to summarise available data on epigenetic changes among women suffering from GDM and their progeny, in association with alterations in the microbiome.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.