The effect of vitamin D deficiency on serum sIL-2R, IL-6 and TNF-alpha levels in adults with Type 1 diabetes

Year 2015, Volume: 42 Issue: 4, 432 - 437, 08.01.2016

Mehmet Türken Sedat Yılmaz , Leyla Çolpan Belkis Aydınol Alpaslan Tuzcu

Abstract

Objective: The aim of this study was to investigate the role of vitamin D deficiency in DMT1 pathogenesis by examining the effects of vitamin D levels on immune modulatory cytokines in patients with DMT1.

Methods: Thirty adults with DMT1 from the endocrine clinic and 30 healthy controls were included in the study. Measurements for 25-hydroxyvitamin D (25OHD), soluble interleukin-2 receptor (sIL-2R), interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α) levels were obtained from serum samples from each study participant. Measurements were compared between the control group and the patient group. Correlations between 25OHD levels and the levels of sIL-2R, IL-6, and TNF-α cytokines were investigated in patients with DMT1.

Results: The mean 25OHD value for the DMT1 patients was significantly lower than for the control group (14.9±9.8 ng/ml versus 24.8±9.4 ng/ml, respectively; p<0.01). The mean sIL-2R and TNF-α scores for patients with DMT1 were significantly higher than for the control group (707.3 ± 265 U/mL versus 403.1 ± 128 U/mL, respectively; p<0.01; and 10.2±3.0 pg/mL versus 3.8 ± 1.6 pg/mL, respectively; p<0.01). There was no significant difference between the mean IL-6 scores of the DMT1 patients and the controls (3.7±1.5 pg/mL versus 4.6±1.3 pg/mL, respectively; p=0,202). Negative correlations with varying levels of significance were observed between 25OHD and sIL-2R, IL-6, and TNF-α cytokine levels in patients with DMT1.

Conclusion: Vitamin D deficiency in DMT1 patients may contribute to disease pathogenesis by increasing sIL-2R, IL-6, and TNF-α cytokines.

Key words: Diabetes mellitus type 1, vitamin D deficiency, soluble interleukin-2 receptor, interleukin-6, tumor necrosis factor-α

Keywords

Tip1 diyabetes mellitus, D vitamini eksikliği, solubl interlökin-2 reseptör, interlökin-6, tümör nekrozis faktör alfa-α

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