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Updated: Jun 2, 2025
Modeling and Evaluation of Murine Diabetic Cardiomyopathy Model
Published on: November 29, 2024
Protective Effect of Vitamin D Supplementation Against Atherosclerotic Cardiovascular Disease in Type 1 Diabetes
1Department of Clinical Laboratory Sciences, College of Applied Medical Sciences, Taif University, Taif, 24227, 20006, Saudi Arabia.
Insights
Vitamin D supplementation significantly improved cardiovascular health in diabetic mice by lowering blood glucose and lipid levels. This study highlights vitamin D
Area of Science:
- Endocrinology
- Immunology
- Cardiovascular Science
Background:
- Cardiovascular disease (CVD) is a primary global cause of mortality, disproportionately affecting men.
- Vitamin D's potential protective role against CVD warrants investigation.
Purpose of the Study:
- To investigate the cardioprotective effects of vitamin D supplementation in a type 1 diabetic mouse model.
- To assess the impact of vitamin D on metabolic markers, cardiac enzymes, and immune cell populations.
Main Methods:
- A cohort of 30 mice was divided into control, diabetic, and vitamin D-treated diabetic groups.
- Key parameters measured included blood glucose, HbA1c, lipid profile, cardiac enzymes (troponin I), adropin, nitric oxide (NO), endothelin-1, VEGF, and various lymphocyte subsets (CD3+, CD4+, CD8+, CD25+).
Main Results:
- Vitamin D treatment significantly reduced blood glucose, HbA1c, lipid profile, cardiac enzymes, endothelin-1, and VEGF in diabetic mice.
- Adropin and NO levels increased with vitamin D treatment.
- Vitamin D modulated lymphocyte populations, decreasing total lymphocytes, CD4+, and CD8+ cells while increasing CD3+ cells, and reducing CD4+CD25+ and CD8+CD25+ populations.
Conclusions:
- Vitamin D supplementation supports cardiovascular integrity by improving glycemic control and lipid profiles.
- Vitamin D demonstrates anti-inflammatory effects, potentially preventing atherosclerotic CVD.
Introduction:
Cardiovascular disease (CVD) is a leading cause of mortality on a global scale, with a higher prevalence observed among men. This study investigated the protective effect of vitamin D supplementation on CVD.
Methods:
A cohort of thirty mice was divided into three groups: control, T1 diabetic, and T1 diabetic groups that received vitamin D treatment. For each mouse in the three groups, measurements were taken of body weight, blood glucose levels, glycated hemoglobin (HbA1c), lipid profile, cardiac enzymes, troponin I, adropin, nitric oxide (NO), endothelin-1, and Vascular endothelial growth factor (VEGF). In addition, measurements were taken for the overall lymphocyte count, as well as the CD3+, CD4+, CD8+, CD4+, CD25+, and CD8+ CD25+ cell counts in all mice.
Results:
The diabetic mice that received vitamin D treatment exhibited significant reductions in blood glucose levels, HbA1c levels, lipid profile, cardiac enzymes, troponin I, endothelin-1, and VEGF levels as compared to the untreated diabetic group (p < 0.01). Furthermore, there was an observed rise in adropin and NO levels in diabetic mice that received vitamin D treatment compared to the untreated diabetic group (p < 0.05). The diabetic mice treated with vitamin D exhibited a substantial decrease in total lymphocyte counts compared to the untreated diabetic and control animals (p < 0.0001). Regarding the CD3+ subset, it was shown that diabetic mice subjected to vitamin D treatment had notably elevated levels of these cells compared to both the untreated diabetic and control groups (p < 0.0001). In addition, the administration of vitamin D resulted in a substantial decrease in the numbers of CD4+ and CD8+ cells in the group of individuals with diabetes (p < 0.0001). The diabetes group that received vitamin D treatment had significantly reduced populations of CD4+ CD25+ and CD8+ CD25+ compared to the untreated diabetic group (p < 0.0001).
Conclusion:
Vitamin D maintains the integrity of the cardiovascular system through the reduction of blood glucose levels and lipid profile. Moreover, its supplementation prevents atherosclerotic CVD by suppressing inflammatory reactions.
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