1654-P: Low Dietary Vitamin D Leads to Glucose Abnormalities in an Obese Animal Model

Introduction: Both obesity and type 2 diabetes (T2D) are linked to vitamin D deficiency. However, we have limited understanding of the role of vitamin D in feeding and glucose homeostasis among its vast target tissues. Furthermore, using the storage form of vitamin D may not be an accurate indicator of vitamin D status in individuals with obesity. Thus, measuring expression levels of vitamin D receptor (VDR)-target genes may be a more promising marker for vitamin D status. The aim of this study was to elucidate the impact of vitamin D on feeding and glucose homeostasis in the context of VDR-target gene expression across multiple tissues. Methods: We fed C57/BJ mice high-fat diets (58% fat) with low (100 IU/kg), regular (1000 IU/kg), or high (5000 IU/kg) vitamin D content. After 18 weeks, we performed an intraperitoneal glucose (1.0 g/kg D20W) tolerance test (GTT). After 26 weeks, we obtained blood samples for liver function testing. qPCR was performed for Insr, and Glut-4 in subcutaneous adipose tissue (SAT) and liver tissue. Results: Mice fed a low-D diet had higher blood glucoses than the regular and high-D groups during GTT (p0.05). Mice fed a low-D diet had worsened liver function compared to the regular and high-D groups (p