Key result
Vitamin D3 improves endothelium-dependent relaxation and preserves aortic contractile responses in diabetic rats.
Why the study?
Type 2 diabetes impairs vascular function and endothelium-dependent vasodilation, but the effects of vitamin D3 on aortic vascular reactivity needed evaluation.
Does Vitamin D3 improve ex vivo aortic vascular reactivity in male Wistar rats with induced Type 2 Diabetes Mellitus?
Does Vitamin D3 improve ex vivo aortic vascular reactivity in male Wistar rats with induced Type 2 Diabetes Mellitus?
Vitamin D3 supplementation restores endothelial function and improves vascular reactivity in an experimental rat model of Type 2 Diabetes Mellitus.
Answers are grounded in this paper and cite their sources.
Hypothesis-generating in diabetic rat model; should not change practice pending human trials.
Background/Objectives: Type 2 Diabetes Mellitus (T2DM) is characterized by insulin resistance and chronic hyperglycemia, which significantly impair vascular function. In experimental T2DM models, the vascular endothelium is compromised, showing decreased vasodilator responses. Vitamin D3 has emerged as a promising intervention for improving glycemic parameters and restoring endothelial function. This study evaluated the effects of vitamin D3 (0.25 and 0.50 µg/kg/day) administered for 4 and 8 weeks on the ex vivo aortic vascular reactivity of T2DM rats. Methods: T2DM was induced in male Wistar rats via a high-fat, normoprotein diet and streptozotocin (30 mg/kg, i.p.). Groups included normal control, diabetic control, metformin, and vitamin D3 (0.25 or 0.50 µg/kg/day). Following 4 or 8 weeks of treatment, thoracic aortic segments were isolated for ex vivo vascular reactivity studies to assess responses to vasoconstrictor and vasorelaxant agents. Results: Vitamin D3 treatment improved glycemic profiles; the 0.25 µg/kg dose reduced fasting glucose, while the 0.50 µg/kg dose lowered glycated hemoglobin at 8 weeks. Endothelium-dependent relaxation induced by acetylcholine was significantly increased in diabetic rats treated with vitamin D3 at both doses over 4 weeks compared to diabetic controls. Moreover, vitamin D3 prevented the attenuation of maximal contractile responses to phenylephrine observed in untreated diabetic rats at 8 weeks. Conclusions: Vitamin D3 supplementation restores endothelial function and improves vascular reactivity in an experimental T2DM model. These findings suggest that vitamin D3 may mitigate vascular complications by enhancing vasorelaxation and maintaining contractile integrity.
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Oliveira et al. (2026) studied Type 2 Diabetes Mellitus. Vitamin D3 vs. diabetic control was evaluated on ex vivo aortic vascular reactivity (endothelium-dependent relaxation and maximal contractile responses). Vitamin D3 supplementation increased endothelium-dependent relaxation and prevented the attenuation of maximal contractile responses in diabetic rats.
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