Vitamin D Supplementation Reduces Both Oxidative DNA Damage and Insulin Resistance in the Elderly with Metabolic Disorders

Abstract

Research evidence indicates that vitamin D deficiency is involved in the pathogenesis of insulin resistance (IR) and associated metabolic disorders including hyperglycemia and dyslipidemia. It also suggested that vitamin D deficiency is associated with elevated levels of oxidative stress and its complications. Therefore, the aim of our study was to determine the effect of vitamin D supplementation on DNA damage and metabolic parameters in vitamin D deficient individuals aged >45 with metabolic disorders. Material and Methods: Of 98 initially screened participants, 92 subjects deficient in vitamin D were included in the study. They were randomly assigned to the following group: with vitamin D supplementation (intervention group, n = 48) and without supplementation (comparative group, n = 44). The patients from both groups were divided into two subgroups according to the presence or absence of type 2 diabetes (T2DM). The intervention group was treated with 2000 International Unit (IU) cholecalciferol/day between October and March for three months. At baseline and after three-month supplementation vitamin D concentration (25-OH)D3 and endogenous and oxidative DNA damage were determined. In addition, fast plasma glucose (FPG), fasting insulin, HbA1c and lipid fraction (total cholesterol (TC), low-density lipoprotein cholesterol (LDL), high-density lipoprotein cholesterol (HDL), triglyceride (TG)), as well as anthropometric measurements (weight, height) were gathered. The following IR-related parameters were calculated Homeostatic Model Assesment - Insulin Resistance (HOMA-IR) and TG/HDL ratio. Results: Three-month vitamin D supplementation increased the mean vitamin D concentration to generally accepted physiological level independently of T2DM presence. Importantly, vitamin D exposure decreased the level of oxidative DNA damage in lymphocytes of patients of intervention group. Among studied metabolic parameters, vitamin D markedly increased HDL level, decreased HOMA-IR, TG/HDL ratio. Furthermore, we found that HbA1c percentage diminished about 0.5% in T2DM patients supplemented with vitamin D. Conclusion: The current study demonstrated that daily 2000I U intake of vitamin D for three months decreased the level of oxidative DNA damage, a marker of oxidative stress, independently on T2DM presence. Furthermore, vitamin D reduced metabolic parameters connected with IR and improved glucose and lipid metabolism. Therefore, our results support the assertion that vitamin D, by reducing oxidative stress and improving of metabolic profile, may decrease IR and related diseases.

Keywords: endogenous and oxidative DNA damage; insulin resistance; lipid profile; type 2 diabetes; vitamin D.

Figure 1

The serum level of vitamin D detected in the intervention group (+Vit. D, n = 48) and the comparative group (−Vit. D, n = 44) before and after three-month supplementation. Results are presented as mean ± standard deviation (SD) (*** p < 0.001).

Figure 2

The serum level of vitamin D detected in patients with type 2 diabetes (T2DM) (T2DM + Vit. D, n = 18; T2DM – Vit. D, n = 14) and patients without T2DM (Control + Vit. D, n = 30; Control − Vit. D, n = 30) before and after three-month supplementation. Results are presented as mean ± SD (* p < 0.05; *** p < 0.001).

Figure 3

The impact of three-month supplementation of vitamin D on the level of endogenous and oxidative DNA damage in the intervention group (+Vit. D, n = 48) in relation to the comparative group (−Vit. D, n = 44). The level of DNA damage was measured by the alkaline comet assay. Data are expressed as mean ± SEM. * p < 0.05; ** p < 0.01.

Figure 4

The impact of three-month supplementation with vitamin D on the level of endogenous and oxidative DNA damage. DNA damage were determined in (A) T2DM patients treated with vitamin D (T2DM + Vit. D, n = 14), (B) T2DM patients not treated with vitamin D (T2DM − Vit. D, n = 18), (C) patients without T2DM treated with vitamin D (Control + Vit.D, n = 30), (D) patients without T2DM not treated with vitamin D (Control − Vit. D, n = 30). The level of DNA damage was measured by the alkaline comet assay. Data are expressed as mean ± SEM. * p < 0.05; ** p < 0.01.

Figure 5

Patient flow diagram.