ArticleBirth defects research. Part A, Clinical and molecular teratology2012
Responses of the embryonic epigenome to maternal diabetes.
Article in Birth defects research. Part A, Clinical and molecular teratology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 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.
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Who cites it
23 citing papers in PubMed, 41 citations in OpenAlex.
- Article
- A Review of the Effects of Maternal and Paternal Obesity on Neurodevelopmental Disorders and Related Neurobiology in Rodent and Human Offspring.Obesity reviews : an official journal of the International Association for the Study of Obesity · 2026Review
- GDM as a unique pathophysiological entity or a transitional pregnancy-induced glucose metabolism abnormality identifying primary diabetes types?Frontiers in physiology · 2026Review
- Prenatal Glucose Intolerance and Child Neurodevelopmental Disorders.JAMA network open · 2025Article
- Association of cumulative social risk and gestational diabetes mellitus in the US, 2007-2018.Diabetes research and clinical practice · 2023Article
- Aberrant lipid accumulation in the mouse visceral yolk sac resulting from maternal diabetes and obesity.Frontiers in cell and developmental biology · 2023Article
- Differential responses to maternal diabetes in embryo and visceral yolk sac.Frontiers in cell and developmental biology · 2023Article
- Epigenetic Changes in Gestational Diabetes Mellitus.International journal of molecular sciences · 2021Review
- Metabolic Profiling in Blastocoel Fluid and Blood Plasma of Diabetic Rabbits.International journal of molecular sciences · 2020Article
- Identification of histone acetylation markers in human fetal brains and increased H4K5ac expression in neural tube defects.Molecular genetics & genomic medicine · 2019Article
- Intergenerational Metabolic Syndrome and Neuronal Network Hyperexcitability in Autism.Trends in neurosciences · 2019Review
- Epigenetics and developmental origins of diabetes: correlation or causation?American journal of physiology. Endocrinology and metabolism · 2018Review
- Effect of diabetes status and hyperglycemia on global DNA methylation and hydroxymethylation.Endocrine connections · 2017Article
- Maternal Factors that Induce Epigenetic Changes Contribute to Neurological Disorders in Offspring.Genes · 2017Review
- Diabetes consequences in the fetus liver of the non-obese diabetic mice.Nutrition & diabetes · 2017Article
- The status of diabetic embryopathy.Upsala journal of medical sciences · 2016Review
- A mutation in the tuft mouse disrupts TET1 activity and alters the expression of genes that are crucial for neural tube closure.Disease models & mechanisms · 2016Article
- The effect of maternal diabetes on the Wnt-PCP pathway during embryogenesis as reflected in the developing mouse eye.Disease models & mechanisms · 2015Article
- Epigenetics and life-long consequences of an adverse nutritional and diabetic intrauterine environment.Reproduction (Cambridge, England) · 2014Review
- Gene expression in teratogenic exposures: a new approach to understanding individual risk.Reproductive toxicology (Elmsford, N.Y.) · 2014Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Maternal diabetes and obesity are independent risk factors for neural tube defects, although it is unclear whether the effects are mediated by common pathogenic mechanisms. In this manuscript, we report a genome-wide survey of histone acetylation in neurulation stage embryos from mouse pregnancies with different metabolic conditions: maternal diabetes, and maternal consumption of a high fat content diet. We find that maternal diabetes, and independently, exposure to high-fat diet, are associated with increases and decreases of H3 and H4 histone acetylation in the embryo. Intriguingly, changes of H3K27 acetylation marks are significantly enriched near genes known to cause neural tube defects in mouse mutants. These data suggest that epigenetic changes in response to diet and metabolic condition may contribute to increased risk for neural tube defects in diabetic and obese pregnancies. Importantly, the responses to high-fat diet and maternal diabetes were distinct, suggesting that perturbed embryonic development under these conditions is mediated by different molecular pathways. This conclusion is supported by morphometric analyses that reveal a trend for maternal diabetes to delay embryonic development in the C57BL/6 strain, while high-fat diet appears to be associated with accelerated development. Taken together, our results link changes in histone acetylation to metabolic conditions during pregnancy, and implicate distinct epigenetic mechanisms in susceptibility to neural tube defects under conditions of maternal diabetes and obesity.
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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.