Key result
Vitamin D3 deficiency is linked to ~2.1-fold higher odds of vascular stiffness.
Why the study?
The role of vitamin D3 deficiency in the development of arterial-wall changes and its relationship with telomere biology in patients with varying insulin sensitivity is not well understood.
Cross-Sectional (n=305)
Odds Ratio: 2.11
p-value: p=0.017
May link vitamin D3 status to cardiometabolic risks in older adults; leaves open causality and practice change pending prospective trials.
The impact of vitamin D3 deficiency on the risk and prognosis of numerous chronic diseases has been actively studied for years. Recent research demonstrates that vitamin D is not merely involved in controlling calcium– phosphorus metabolism, but can also enhance insulin sensitivity, and decrease the incidence of type-2 diabetes mellitus (T2DM), obesity, and the autoimmune destruction of pancreatic β cells. The influence of vitamin D3 on some cardiometabolic risk factors and cardiovascular disease (CVD) is described. Thus, it seems quite relevant to study the role of vitamin D3 in the development of arterial-wall changes in the case of T2DM and insulin resistance (IR) and their relationship with the biology of telomeres. The study is aimed at investigating the relationship between vitamin D3 deficiency and vascular-wall condition by the telomere biology in patients with varying insulin sensitivity. The cross-sectional study involves 305 patients (106 men and 199 women) aged 51.5 ± 13.3 SU. All patients undergo laboratory and instrumental tests; the morphofunctional state of the vascular wall is studied. The telomere length and telomerase activity are determined using polymerase chain reaction. Altogether 18 out of 248 patients (7.2%) are found to have normal vitamin D3 levels (above 30 ng/mL). Vitamin D3 insufficiency or deficiency is determined in 92.8% of subjects. The increase in the vitamin D3 deficiency is accompanied by an increased level of fasting glucose, HbA1c and its elevated concentration, HOMA index, glucose disorders up to T2DM, and higher vascular stiffness. Telomerase activity in the group with vitamin D3 deficiency is significantly lower than in the groups with vitamin D3 insufficiency and normal concentrations. Multiple linear regression analysis shows that they are independently associated with vitamin D3 in T2DM (B = 1.43; st. OR 0.106; p = 0.0001), vascular stiffness (B = 0.075; st. OR 2.11; p = 0.017), fasting glucose (B = 0.169; st. OR 1.62; p = 0.004), HbA1c level (B = 0.062; st. OR 7.4; p = 0.001) and the presence of “short” telomeres (B = 0.09; st. OR 1.154; p = 0.001). Receiver-operating characteristic (ROC) analysis reveals relationships between the BMI (0.634, p = 0.001), duration of T2DM (0.651, p = 0.022), high intima-media thickness (0.614, p = 0.004), vascular stiffness (0.605, p < 0.001), HbA1c (0.588, p = 0.022), and the presence of vitamin D3 deficiency. In persons with varying insulin sensitivity, from insulin resistance to T2DM, it is advisable to assess the vitamin D3 levels for effective prevention of arterial-wall changes in addition to traditional CVD risk factors. Vitamin D3 deficiency requires the active prevention of metabolic disorders and vascular changes.
No takes yet. Share an insight, caveat, or question.
Dudinskaya et al. (2023) conducted a cross-sectional in Insulin resistance and type 2 diabetes mellitus (n=305). Vitamin D3 deficiency vs. Vitamin D3 insufficiency and normal concentrations was evaluated on Vascular stiffness (OR 2.11, p=0.017). Vitamin D3 deficiency was associated with increased vascular stiffness (OR 2.11; P=0.017), higher HbA1c (OR 7.4; P=0.001), and the presence of short telomeres (OR 1.154; P=0.001).
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: