Effect of vitamin D replacement on endothelial function and oxidative stress in vitamin D deficient subjects
Ozlem Tarcin1, Dilek Yavuz1, Ahmet Toprak2, Ahu Telli3, Meral Yuksel4, Dilek Yazici1, Seda Sancak1, Oguzhan Deyneli1, Goncagul Haklar3 & Sema Akalin1
Introduction: Vitamin D (Vit D) receptors have been shown in extra skeletal tissues. Vit D deficiency plays a role in the development of many malignant, chronic inflammatory, autoimmune and metabolic diseases. Our aim was to evaluate the effect of Vit D replacement therapy on insulin sensitivity, endothelial function and oxidative stress in Vit D deficient subjects.
Material-method: Serum 25(OH) D levels of 74 volunteer-healthy subjects (22.7±2.7) were screened. Twenty subjects (22.6±2.1) with 25(OH) D levels < 20 ng/ml were recruited as deficient group (D) and 20 subjects (23±2.3) with 25(OH) D levels >40 ng/ml were selected as control group (C). Monthly 300 000 IU Vit D was injected for 3 months to group D. Before and after 3 months, blood samples were collected for serum Ca, P, iPTH, thiobarbituric acid reactive substance (TBARs) and paraoxonase. Endothelial function was evaluated by measuring flow mediated dilatation (FMD) from brachial artery. Insulin sensitivity index was calculated according to 75gr OGTT.
Results: In group D, basal TBARs levels were higher compared to group C and decreased after Vit D therapy (Table 1). Basal FMD of group D were found to be lower than group C and increased after therapy. We found negative correlation between FMD and TBARs (P=0.001; r=−0.51) in group D. After therapy, 30th sec. insulin level increased during OGTT.
Table 1 Parameters before and after replacement therapy
| ||Before therapy||After therapy||Control|
|*P<0.05 before and after therapy; **P<0.05 before therapy and control|
Discussion: We have shown that vit D deficiency causes endothelial dysfunction. Vit D replacement led to the improvement on endothelial function and decreased lipid peroxidation which made us think that vit D deficiency could have take part in the pathogenesis of atherosclerosis.