ArticleThe Journal of biological chemistry2008
Histone code modifications repress glucose transporter 4 expression in the intrauterine growth-restricted offspring.
Article in The Journal of biological chemistry, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT02211651 (Maternal Adipose Tissue and Placental Dysfunction Programs the Fetus for Type 2 Diabetes), which is not on this map. Cited by 88 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Maternal Adipose Tissue and Placental Dysfunction Programs the Fetus for Type 2 Diabetes (PlacentA-DM)
Who cites it
88 citing papers in PubMed, 221 citations in OpenAlex.
- The Potential Physiologic Mechanisms by Which Early-Life Nutrition May Influence Type 2 Diabetes Pathophysiology in Humans.Annual review of nutrition · 2026Review
- Decoding type 5 diabetes using spatial omics: microarchitectural and molecular mechanisms of malnutrition-associated diabetes.Frontiers in endocrinology · 2026Review
- Adipocyte RNF20 Knockout Leads to Hyperinsulinemia via the H2Bub-H3K4me3-Slc2a4 Axis.Journal of cellular and molecular medicine · 2025Article
- HDAC4: an emerging target in diabetes mellitus and diabetic complications.European journal of medical research · 2025Review
- Maternal Protein Restriction Inhibits Insulin Signaling and Insulin Resistance in the Skeletal Muscle of Young Adult Rats.Juntendo Iji zasshi = Juntendo medical journal · 2024Article
- MeCP2 Is an Epigenetic Factor That Links DNA Methylation with Brain Metabolism.International journal of molecular sciences · 2023Review
- Current Knowledge on the Pathophysiology of Lean/Normal-Weight Type 2 Diabetes.International journal of molecular sciences · 2022Review
- Maternal Calorie Restriction Induces a Transcriptional Cytoprotective Response in Embryonic Liver Partially Dependent on Nrf2.Antioxidants (Basel, Switzerland) · 2022Article
- Maternal low protein diet and fetal programming of lean type 2 diabetes.World journal of diabetes · 2022Review
- Regulation of Pancreatic β-Cell Mass by Gene-Environment Interaction.Diabetes & metabolism journal · 2022Review
- Diabetes: discovery of insulin, genetic, epigenetic and viral infection mediated regulation.The Nucleus : an international journal of cytology and allied topics · 2022Review
- Going Up Inflame: Reviewing the Underexplored Role of Inflammatory Programming in Stress-Induced Intrauterine Growth Restricted Livestock.Frontiers in animal science · 2021Article
- Review
- Molecular mechanisms governing offspring metabolic programming in rodent models of in utero stress.Cellular and molecular life sciences : CMLS · 2020Review
- Epigenetic modification and therapeutic targets of diabetes mellitus.Bioscience reports · 2020Review
- Altered Transcription Factor Binding and Gene Bivalency in Islets of Intrauterine Growth Retarded Rats.Cells · 2020Article
- Suppression of HDAC by sodium acetate rectifies cardiac metabolic disturbance in streptozotocin-nicotinamide-induced diabetic rats.Experimental biology and medicine (Maywood, N.J.) · 2020Article
- Epigenetic Regulation by Dietary Restriction: Part II.Conditioning medicine · 2019Article
- Genomic imprinting and its effects on postnatal growth and adult metabolism.Cellular and molecular life sciences : CMLS · 2019Review
- Epigenetic disturbances in obesity and diabetes: Epidemiological and functional insights.Molecular metabolism · 2019Review
28 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
We examined transcriptional and epigenetic mechanism(s) behind diminished skeletal muscle GLUT4 mRNA in intrauterine growth-restricted (IUGR) female rat offspring. An increase in MEF2D (inhibitor) with a decline in MEF2A (activator) and MyoD (co-activator) binding to the glut4 promoter in IUGR versus control was observed. The functional role of MEF2/MyoD-binding sites and neighboring three CpG clusters in glut4 gene transcription was confirmed in C2C12 muscle cells. No differential methylation of these three and other CpG clusters in the glut4 promoter occurred. DNA methyltransferase 1 (DNMT1) in postnatal, DNMT3a, and DNMT3b in adult was differentially recruited with increased MeCP2 (methyl CpG-binding protein) concentrations to bind the IUGR glut4 gene. Covalent modifications of the histone (H) code consisted of H3.K14 de-acetylation by recruitment of histone deacetylase (HDAC) 1 and enhanced association of HDAC4 enzymes. This set the stage for Suv39H1 methylase-mediated di-methylation of H3.K9 and increased recruitment of heterochromatin protein 1alpha, which partially inactivates postnatal and adult IUGR glut4 gene transcription. Further increased interactions in the adult IUGR between DNMT3a/DNMT3b and HDAC1 and MEF2D and HDAC1/HDAC4 and decreased association between MyoD and MEF2A existed. We conclude that epigenetic mechanisms consisting of histone code modifications repress skeletal muscle glut4 transcription in the postnatal period and persist in the adult female IUGR offspring.
Indexed as
Identifiers
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.