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Cardiomyopathy in offspring of pregestational diabetic mouse pregnancy
Daniel Dowling1, Niamh Corrigan1, Stephen Horgan2
1UCD Obstetrics & Gynaecology, School of Medicine and Medical Science, National Maternity Hospital, University College Dublin, Dublin 2, Ireland ; UCD Conway Institute of Biomolecular and Biomedical Research, University College Dublin, Belfield, Dublin 4, Ireland.
Insights
Maternal diabetes during pregnancy leads to increased collagen and cardiomyocyte nuclei in offspring hearts during gestation. These cardiac changes in offspring normalize after birth, suggesting the intrauterine environment is key.
Area of Science:
- Cardiovascular Research
- Developmental Biology
- Endocrinology
Background:
- Maternal diabetes mellitus poses risks to fetal development.
- Type 1 diabetes during pregnancy can impact offspring cardiovascular health.
- Understanding gestational diabetes effects on fetal heart development is crucial.
Purpose of the Study:
- To investigate cardiomyopathy in offspring from a mouse model of pregestational type 1 diabetic pregnancy.
- To assess the impact of maternal diabetes on fetal and postnatal cardiac development.
Main Methods:
- Induced pregestational diabetes in female C57BL6/J mice using STZ.
- Examined offspring at embryonic day 18.5, 6 weeks, and 12 weeks.
- Quantified cardiomyocyte nuclei size/number and collagen deposition via digital image analysis of stained cardiac tissue.
Main Results:
- Embryonic offspring (day 18.5) from diabetic mothers showed increased cardiomyocyte nuclei number (hyperplasia) and smaller nuclei size.
- Significantly increased collagen deposition was observed in the hearts of embryonic offspring from diabetic mothers.
- No significant cardiac differences were found between diabetic and control offspring at 6 and 12 weeks postpartum.
Conclusions:
- Offspring of type 1 diabetic mice exhibit increased myocardial collagen and cardiomyocyte hyperplasia in late gestation.
- These gestational cardiac alterations normalize postpartum, indicating resolution after leaving the maternal intrauterine environment.
- The intrauterine environment plays a critical role in mediating gestational diabetes-induced cardiac changes in offspring.
Purpose:
To investigate cardiomyopathy in offspring in a mouse model of pregestational type 1 diabetic pregnancy.
Methods:
Pregestational diabetes was induced with STZ administration in female C57BL6/J mice that were subsequently mated with healthy C57BL6/J males. Offspring were sacrificed at embryonic day 18.5 and 6-week adolescent and 12-week adult stages. The size and number of cardiomyocyte nuclei and also the extent of collagen deposition within the hearts of diabetic and control offspring were assessed following cardiac tissue staining with either haematoxylin and eosin or Picrosirius red and subsequently quantified using automated digital image analysis.
Results:
Offspring from diabetic mice at embryonic day 18.5 had a significantly higher number of cardiomyocyte nuclei present compared to controls. These nuclei were also significantly smaller than controls. Collagen deposition was shown to be significantly increased in the hearts of diabetic offspring at the same age. No significant differences were found between the groups at 6 and 12 weeks.
Conclusions:
Our results from offspring of type 1 diabetic mice show increased myocardial collagen deposition in late gestation and have increased myocardial nuclear counts (hyperplasia) as opposed to increased myocardial nuclear size (hypertrophy) in late gestation. These changes normalize postpartum after removal from the maternal intrauterine environment.
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