Abstract
Vitamin D deficiency is highly prevalent in patients with overweight/obesity and type 2 diabetes (T2DM). Herein, we investigated the relationship between vitamin D status and overweight/obesity status, insulin resistance (IR), systemic inflammation as well as oxidative stress (OS). Anthropometric and laboratory assessments of 25-hydroxyvitamin D (25(OH)D) and glycemic, pro-inflammatory and OS biomarkers were performed in a sample of 47 patients with T2DM who were divided into categories based on overweight and degree of obesity. The main findings were: the overweight/obesity status correlated negatively with the degree of serum 25(OH)D deficiency (ρ = −0.27) with a trend towards statistical significance (p = 0.069); the homeostasis model assessment of insulin resistance (HOMA-IR) was significantly different (p = 0.024) in patients with 25(OH)D deficiency, as was total oxidant status (TOS) and oxidative stress index (OSI) in patients with severe serum 25(OH)D deficiency as compared to those with 25(OH)D over 20 ng/mL (TOS: p = 0.007, OSI: p = 0.008); and 25(OH)D had a negative indirect effect on TOS by body mass index (BMI), but BMI was not a significant mediator of the studied relationship. In a setting of overweight and increasing degree of obesity, patients with T2DM did not display decreasing values of 25(OH)D. Subjects with the lowest values of 25(OH)D presented the highest values of BMI. Patients with 25(OH)D deficiency were more insulin resistant and showed increased OS but no elevated systemic inflammation. The negative effect of 25(OH)D on TOS did not seem to involve BMI as a mediator.
Highlights
Emerging data have depicted vitamin D deficiency as a hallmark of obesity [1,2] significantly lower serum vitamin D levels, as assessed by serum 25-hydroxyvitaminD (25(OH)D), have been reported in obese as compared to lean subjects [3,4]
We found no significant differences in the blood glucose (p > 0.05) or in the lipid profile and inflammatory status in the studied groups (Table 1)
GM = geometric mean; AM = arithmetic mean; ME = median point estimation; one-way ANOVA or Kruskal–Wallis test; 95% confidence intervals (CI) for the geometric mean are calculated in the traditional manner with the t-distribution; 95% confidence intervals (CI) for the median are calculated by the percentile method with 10,000 bootstrap samples; * statistically significant result: p < 0.05; ** statistically very significant result: p < 0.01; 25(OH)D: serum 25-hydroxyvitamin D; BMI: body mass index; HOMA-IR: homeostasis model assessment of insulin resistance; IL-6: interleukin 6; NOx : nitrites/nitrates; TOS: total oxidant status; TAR: total antioxidant response; OSI: oxidative stress index
Summary
Emerging data have depicted vitamin D deficiency as a hallmark of obesity [1,2] significantly lower serum vitamin D levels, as assessed by serum 25-hydroxyvitaminD (25(OH)D), have been reported in obese as compared to lean subjects [3,4]. Obesity itself comprises several pathological features such as impaired insulin signaling, beta cell dysfunction, low-grade chronic inflammation and oxidative stress, which all result in insulin resistance (IR), and in type 2 diabetes mellitus onset (T2DM) [11]. The relationship between vitamin D deficiency, obesity and T2DM as well as their underlying mechanisms, i.e., insulin-resistance (IR), low-grade systemic inflammation and oxidative stress is more complex and needs further investigation as studies report conflicting results [15]. A negative association between serum 25(OH)D and several biomarkers of systemic inflammation has been reported by several authors [23], regardless of the total quantity of fat mass, whereas others have showed no relationship between these parameters, which points to the lack of involvement of 25(OH)D in the pro-inflammatory milieu in obese individuals [24]
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