Maternal voluntary exercise mitigates oxidative stress and incidence of congenital heart defects in pre-gestational diabetes
Open accessAbstract
Women with pre‐gestational diabetes have a higher risk of producing children with congenital heart defects (CHDs), caused predominantly by hyperglycemia‐induced oxidative stress. In this study, we evaluated if exercise during pregnancy could mitigate oxidative stress and reduce the incidence of CHDs in the offspring of diabetic mice. Female mice were treated with streptozotocin to induce pre‐gestational diabetes, then mated with healthy males to produce offspring. They were also given access to running wheels 1 week before mating and allowed to exercise voluntarily until E18.5. Heart morphology, gene expression, and oxidative stress were assessed in foetal hearts. Maternal voluntary exercise results in a significantly lower incidence of CHDs from 59.5% to 25%. Additionally, diabetes‐induced defects in coronary artery and capillary morphogenesis were also lower with exercise. Myocardial cell proliferation and epithelial‐mesenchymal transition at E12.5 was significantly lower with pre‐gestational diabetes which was mitigated with maternal exercise. Cardiac gene expression of Notch1 , Snail1 , Gata4 and Cyclin D1 was significantly higher in the embryos of diabetic mice that exercised compared to the non‐exercised group. Furthermore, maternal exercise produced lower reactive oxygen species (ROS) and oxidative stress in the foetal heart. In conclusion, maternal exercise mitigates ROS and oxidative damage in the foetal heart, and results in a lower incidence of CHDs in the offspring of pre‐gestational diabetes. Exercise may be an effective intervention to compliment clinical management and further minimize CHD risk in mothers with diabetes.
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One study examined diabetes during pregnancy and showed that maternal voluntary wheel running lowered the incidence of congenital heart defects in the offspring.
“One study examined diabetes during pregnancy and showed that maternal voluntary wheel running lowered the incidence of congenital heart defects in the offspring [139].”
From Recent Experimental Studies of Maternal Obesity, Diabetes during Pregnancy and the Developmental Origins of Cardiovascular Disease (2022) · cites this paper as [139]
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- Authors
- Saiyin, T., Engineer, A., Greco, E. R., Kim, M. Y., Lu, X., Jones, D. L., & Feng, Q.
- Affiliations
- Western University (CA)
- Corresponding author
- Feng, Qingping
- Venue
- Journal of Cellular and Molecular Medicine
- Publisher
- Wiley
- Published
- 2019-06-18
- Volume
- 23
- Issue
- 8
- Pages
- 5553-5565
- ISSN
- 1582-1838 (ISSN-L)
- 1582-4934
- PMC
- PMC6653048
- OpenAlex
- W2952377980
- Cited by
- 47
- References
- 45
- Citations by year
- 2026: 2 · 2025: 8 · 2024: 7 · 2023: 8 · 2022: 10 · 2021: 2 · 2020: 6 · 2019: 3 · 2018: 1
- FWCI
- 1.74
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Journal of Cellular and Molecular Medicine (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Scholarship@Western (Western University) (submittedVersion)
- Funders
- Canadian Institutes of Health Research
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Congenital heart defects research
- Health Sciences › Medicine › Obstetrics and Gynecology › Gestational Diabetes Research and Management
- Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Birth, Development, and Health
- Keywords
- pregestational diabetes, congenital heart disease, oxidative stress, reactive oxygen species, fetal heart development, capillary morphogenesis, epithelial-mesenchymal transition, cardiomyocyte proliferation, Notch1, SNAI1, GATA4, cyclin D1, streptozotocin-induced diabetes, diabetic mice
- MeSH terms
- Animals, Blood Glucose, Capillaries, Coronary Vessel Anomalies, Diabetes Mellitus, Experimental, Embryo, Mammalian, Female, Heart Defects, Congenital, Litter Size, Male, Mice, Inbred C57BL, Pericardium, Phosphorylation, Physical Conditioning, Animal, Pregnancy, Diabetes, Gestational, Oxidative Stress, Gene Expression Regulation, Developmental, Cell Proliferation, Nitric Oxide Synthase Type III, Epithelial-Mesenchymal Transition
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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