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Calcitriol Supplementation Ameliorates Microvascular Endothelial Dysfunction in Vitamin D-Deficient Diabetic Rats by
Chee Lee Wee1, Siti Safiah Mokhtar1, Kirnpal Kaur Banga Singh2
1Department of Pharmacology, School of Medical Sciences, Universiti Sains Malaysia, 16150 Kota Bharu, Kelantan, Malaysia.
Oxidative Medicine and Cellular Longevity
|February 24, 2021
Summary
Vitamin D deficiency in diabetic rats impairs vascular function by reducing nitric oxide synthase and increasing oxidative stress. Supplementation with calcitriol (active vitamin D) reversed these detrimental effects, suggesting a therapeutic role.
Area of Science:
- Endocrinology and Metabolism
- Cardiovascular Physiology
- Nutritional Biochemistry
Background:
- Diabetes mellitus is associated with macro- and microvascular complications, increasing cardiovascular risk.
- Vitamin D deficiency is prevalent in diabetes and may exacerbate vascular dysfunction.
- The role of vitamin D in diabetic microcirculation and oxidative stress requires further investigation.
Purpose of the Study:
- To investigate the impact of vitamin D deficiency on vascular function and oxidative status in the microcirculation of diabetic rats.
- To determine if calcitriol supplementation can reverse these effects in diabetic rats.
Main Methods:
- Streptozotocin-induced diabetic rats were divided into control diet, vitamin D-deficient diet, and vitamin D-deficient diet with calcitriol supplementation groups.
- Mesenteric arterial rings were analyzed for relaxation and contraction responses using wire myography.
- Protein expression of endothelial nitric oxide synthase (eNOS), superoxide dismutase (SOD) activity, and malondialdehyde (MDA) levels were measured.
Main Results:
- Vitamin D deficiency significantly reduced endothelium-dependent relaxation and eNOS expression while increasing oxidative stress markers (MDA) in diabetic rat mesenteric arteries.
- Calcitriol supplementation restored endothelium-dependent relaxation and normalized eNOS expression and oxidative stress markers.
- Vitamin D deficiency worsened endothelium-dependent contraction, an effect not reversed by calcitriol.
Conclusions:
- Vitamin D deficiency contributes to impaired vascular function in diabetes through eNOS downregulation and increased oxidative stress.
- Calcitriol supplementation shows potential in mitigating diabetes-related microvascular complications by improving vascular health.
- This highlights the importance of vitamin D status in managing cardiovascular risks associated with diabetes.
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