Diabetic keratopathy occurs in ∼70% of all people with diabetes. This study was designed to examine the effects of vitamin D receptor knockout (VDR−/−) and vitamin D deficiency (VDD) on corneal epithelial wound healing and nerve density in diabetic mice. Diabetes was induced using the low-dose streptozotocin method. Corneal epithelial wounds were created using an Algerbrush, and wound healing was monitored over time. Corneal nerve density was measured in unwounded mice. VDR−/− and VDD diabetic mice (diabetic for 8 and 20 weeks, respectively) had slower healing ratios than wild-type diabetic mice. VDR−/− and VDD diabetic mice also showed significantly decreased nerve density. Reduced wound healing ratios and nerve densities were not fully rescued by a supplemental diet rich in calcium, lactose, and phosphate. We conclude that VDR−/− and VDD significantly reduce both corneal epithelial wound healing and nerve density in diabetic mice. Because the supplemental diet did not rescue wound healing or nerve density, these effects are likely not specifically related to hypocalcemia. This work supports the hypothesis that low vitamin D levels can exacerbate preexisting ophthalmic conditions, such as diabetes.

中文翻译：

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维生素 D 受体敲除和维生素 D 缺乏对糖尿病小鼠角膜上皮伤口愈合和神经密度的影响

约 70% 的糖尿病患者患有糖尿病性角膜病。本研究旨在探讨维生素 D 受体敲除 (VDR−/−) 和维生素 D 缺乏 (VDD) 对糖尿病小鼠角膜上皮伤口愈合和神经密度的影响。使用低剂量链脲佐菌素方法诱发糖尿病。使用 Algerbrush 创建角膜上皮伤口，并随时间监测伤口愈合情况。测量未受伤小鼠的角膜神经密度。VDR−/− 和 VDD 糖尿病小鼠（分别患有糖尿病 8 周和 20 周）的愈合率比野生型糖尿病小鼠慢。VDR−/− 和 VDD 糖尿病小鼠也表现出神经密度显着降低。富含钙、乳糖和磷酸盐的补充饮食并不能完全挽救伤口愈合率和神经密度的降低。我们得出结论，VDR−/− 和 VDD 显着降低糖尿病小鼠的角膜上皮伤口愈合和神经密度。由于补充饮食不能挽救伤口愈合或神经密度，因此这些影响可能与低钙血症没有特定关系。这项工作支持这样的假设：维生素 D 水平低会加剧糖尿病等已有的眼科疾病。