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Inflammatory protein expression in adolescent and adult offspring of type 1 diabetic mice
Daniel Dowling1, Niamh Corrigan, Paul Downey
1UCD Obstetrics & Gynaecology, School of Medicine and Medical Science, University College Dublin, National Maternity Hospital, Dublin, Ireland.
Insights
Offspring from mothers with pregestational type 1 diabetes exhibit elevated inflammatory markers, including soluble vascular cell adhesion molecule-1 (sVCAM-1) and total plasminogen activator inhibitor-1 (tPAI-1). This suggests a potential mechanism for increased cardiovascular disease risk.
Area of Science:
- Reproductive biology and developmental origins of health and disease.
- Endocrinology and metabolic disorders.
- Immunology and inflammation research.
Background:
- Pregestational type 1 diabetes in mothers poses risks to offspring development.
- Maternal hyperglycemia can impact fetal programming and long-term health outcomes.
- Understanding early-life inflammatory changes is crucial for predicting future health.
Discussion:
- Offspring of diabetic mothers show significantly higher levels of key inflammatory markers in adolescence.
- Specific markers like sVCAM-1 and tPAI-1 are notably elevated, indicating a pro-inflammatory state.
- These inflammatory changes may persist into adulthood, contributing to chronic disease risk.
Key Insights:
- Adolescent offspring of type 1 diabetic mothers have increased levels of Matrix metalloproteinase 9, soluble E-selectin, sICAM-1, sVCAM-1, and tPAI-1.
- A significant rise in sVCAM-1 and tPAI-1 was observed in this offspring group compared to controls.
- These findings highlight early inflammatory alterations in offspring exposed to maternal diabetes in utero.
Outlook:
- The observed inflammation may mediate the increased cardiovascular disease risk in offspring of diabetic mothers.
- Further research can explore targeted interventions to mitigate these inflammatory pathways.
- Longitudinal studies are needed to confirm the long-term health consequences of these early inflammatory changes.
Aims:
To measure inflammatory markers in offspring of pregestational type 1 diabetic mothers.
Methods:
Type 1 diabetes was induced in female C57BL6/J mice using streptozotocin. Offspring from control C57BL6/J and type 1 diabetic mothers were followed up to adulthood and blood was collected at 6 and 12 weeks of age, representing adolescent and adult stages respectively. Five well-established inflammatory markers; Matrix metalloproteinase 9, soluble E-selectin, sICAM-1, sVCAM-1, and total plasminogen activator inhibitor-1 (PAI-1) were measured on an inflammatory multiplex assay in plasma.
Results:
Blood plasma from adolescent offspring from diabetic mothers displayed an increase in all five inflammatory markers when compared to controls, and there was a highly significant increase in sVCAM-1 (64.56 ± 20.1 vs. 33.8 ± 20.75; p < 0.01) and tPAI-1 (0.05 ± 0.02 vs. 0.02 ± 0.01; p < 0.01) expression.
Conclusion:
Our findings show that inflammatory markers are increased in offspring of pregestational diabetic mothers. This may represent a mechanism for increased risk of cardiovascular disease evident in these offspring.
