Conclusion
Serum 25(OH)D was elevated and Vitamin D deficiency enhanced insulin resistance by promoting inflammation via NF-kB pathway in patients with T2DM.
Methods
60 health people and 106 patients with T2DM were measured the level of serum 25(OH)D, fasting blood glucose, insulin, TNF-α, IL-6, IL-8, and IL-1β, etc. We established a rat model of T2DM and vitamin D (VD) deficiency, and studied the effects of VD deficiency on homeostasis model assessment insulin resistance (HOMA-IR) and pancreatic inflammation.
Objective
This study was aimed to analyze the level of serum 25(OH)D in patients with type 2 diabetes (T2DM), and explore the relationship between serum 25(OH)D and insulin resistance.
Results
The level of serum 25(OH)D in patients with T2DM was significantly lower than that in health people, and HOMA-IR decreased with the increasing of the serum 25(OH)D level. Pearson correlation analysis showed that the serum 25(OH)D level in patients with T2DM had a negative correlation with HOMA-IR (r=-0.750, P<0.001), TNF-α (r=-0.705, P<0.001), IL-1β (r=-0.661, P<0.001), IL-8 (r=-0.645, P<0.001), and IL-6 (r=-0.609, P<0.001). In animal experiment, Vitamin D deficiency enhanced HOMA-IR in rats with T2DM and reversed it by supplementing VD. Vitamin D deficiency could increase the inflammatory response by up-regulating p-p65/RelB in the pancreas tissue.