39 - Effects of Vitamin D Receptor Knockout, Vitamin D Deficiency, and Diabetes on Corneal Epithelial Nerve Density

Abstract

It is estimated that 41.6% of the US population suffers from vitamin D deficiency or insufficiency, with Blacks (82.1%) and Hispanics (69.2%) at even greater risk.¹ Vitamin D deficiency can be caused by a variety of sources such as low exposure to sunlight, a strict vegan diet, or inability of the digestive system to absorb vitamins. This project is designed to test the general hypothesis that Vitamin D deficiency exacerbates preexisting primary corneal pathologies. Previous research has established that the corneal epithelium in diabetic mice heals at a faster rate than the epithelium in diabetic vitamin D receptor (VDR) knockout (KO) mice. It is known that within diabetic mice, the corneal nerve density is decreased and it has been hypothesized that the decreased nerve density can slow corneal epithelium healing within mice. However, it is unknown how VDR KO mice or vitamin D deficient with diabetes will affect corneal nerve density. Dr. Watsky’s laboratory has established that each of the previous factors alone slow corneal epithelial wound healing. In order to identify variabilities within the nerves that indicate slow wound healing, the mouse corneas will be collected, stained for confocal microscope observation, and analyzed through image processing to determine nerve density. Thus far, this research has shown a significant difference and decreased nerve density in VDR KO diabetic mice when compared to WT diabetic mice and slight variation in Vitamin D deficient diabetic mice when compared to the WT diabetic as well.

¹Forrest, KY., Stuhldreher, WL. (2011). Prevalence and correlates of vitamin D deficiency in US adults. Nutr Res., 48-54. doi:10.1016/j.nutres.2010.12.001