Endocrine Abstracts

Introduction: It is suggested that hyperuricemia in type 2 diabetes (T2DM) patients causes reactive oxygen species (ROS) accumulation, which causes the destruction of beta cells of the pancreas and contributes to T2DM. This study aimed to analyze the relationship between vitamin D deficiency (which is reciprocally related to Serum Uric Acid (SUA) levels), hyperuricemia, and levels of ROS scavengers in T2DM patients, and to investigate the effect of vitamin D supplementation on these parameters.

Materiel & Methods: The study included 26 T2DM patients with vitamin D deficiency who received vitamin D supplements for three months. HbA1c, insulin, SUA, xanthine oxidase (XO) levels, lipid peroxidation, Glutathione Peroxidase (GPx) activity, GSH/GSSG ratio, and vitamin D levels were measured prior to and after supplementation.

Results: Adenosine deaminase (ADA) and XO levels and activity were elevated in T2DM patients, along with SUA levels. Vitamin D supplementation resulted in significant (P value <.005) decreases in HbA1c, HOMA-IR, SUA, XO levels, ADA levels, and activity, lipid peroxidation, and GPx activity. A significant increase in GSH/GSSG ratio was also observed.

Conclusion: Vitamin D supplementation reduces oxidative stress caused by high levels of uric acid observed in T2DM patients by reducing the activity of ADA and XO enzymes.