It is associated with lower exposure to sunlight and reduced skin synthesis. Another hypothesis is that decreased 25(OH)D 3 levels in obese people are due to a sedentary lifestyle and lack of physical activity. A potential explanation for this phenomenon is vitamin D sequestration in adipose tissue. Many studies have shown that obese people have lower levels of 25(OH)D 3 the serum compared to people of normal weight. It has also been proven that low serum 25(OH)D 3 concentration is associated with endothelial dysfunction and increases inflammation. Vitamin D deficiency likely leads to the development of cardiovascular diseases (CVDs) by an overactive renin–angiotensin–aldosterone system (RAAS). reported that American patients with vitamin D deficiency, defined as serum 25(OH)D 3 levels < 30 ng/ml, reached 60% and significantly correlated with the occurrence of type 2 diabetes, hypertension, coronary heart disease (CHD), myocardial infarction (MI), heart failure (HF) and was associated with higher overall mortality. In the Framingham Offspring Study, which included 1739 subjects without heart disease, the risk of a cardiovascular incident was 53% to 80% higher in subjects with low 25(OH)D 3 levels during a seven-year prospective observation. The pathomechanism of this process is related to impaired NO signalling and endothelium-derived hyperpolarizing factor (EDHF). observed that mesenteric arteries of 25(OH)D 3 deficient rats were characterised by a twofold decrease in their ability to diastole. Inflammation together with oxidative stress promotes impaired vascular perfusion, resulting in an increased risk of coronary artery disease. An undoubted role in the development of atherosclerotic plaque is played by a chronic inflammatory process. There is evidence that vitamin D can modulate the pathogenesis of atherosclerosis. Moreover, the cardioprotective role of this vitamin in patients after myocardial infarction has been described. Many studies have described the importance of vitamin D deficiency in the development of atherosclerosis, coronary heart disease, hypertension, heart failure and atrial fibrillation. The vitamin D receptor (VDR) is located in endothelial cells, vascular smooth muscle and cardiomyocytes. Reducing inflammation and the potential impact on vascular reactivity leads to the conclusion that cholecalciferol supplementation in obese patients may benefit the cardiovascular system. This study indicates that restoring normal 25(OH)D 3 levels in obese people reduces the concentration of pro-inflammatory factors associated with cardiovascular diseases. At the same time, NO and VEGF-A levels increased statistically significantly. A statistically significant reduction leptin and TMAO levels was observed. Normal levels were achieved in most patients. ResultsĪfter supplementation, 25(OH)D 3 levels increased significantly. 25(OH)D 3 levels measured on Beckman Coulter DXI 800 by chemiluminescence method. Concentrations of nitric oxide (NO), vascular endothelial growth factor A (VEGF-A), leptin, trimethylamine N-oxide (TMAO) and soluble suppression of tumorigenicity 2 (sST2) were measured in baseline samples using ELISA (BioTek EPOCH). For three months, the subjects supplemented with cholecalciferol at a dose of 2000 IU/day. The study enrolled 33 obese patients with insufficient 25(OH)D 3 levels. Our study investigates the effect of cholecalciferol supplementation in obese patients on selected biomarkers associated with cardiovascular diseases (CVDs). While the effects of a deficiency on the skeletal or immune system are known, the effects on the cardiovascular system are not yet clear. Obese patients are most at risk of having serum 25-hydroxyvitamin D 3 (25(OH)D 3) levels that are too low due to the accumulation of vitamin D in adipose tissue. Vitamin D deficiency is one of the most common health issues in developed countries.
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