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Summary Background Metabolic syndrome (MetS) patients can have low 25-hydroxyvitamin D 25(OH)VitD levels, which may be associated with increased oxidative stress. There is little data on the effect of 25(OH)VitD administration plus dietary intervention on oxidative stress markers in these patients. Aim To study the effect of 25(OH)VitD administration plus dietary intervention on oxidative stress markers in MetS patients. Methods This is a pre-specified analysis of a previously published study (NCT01237769 ClinicalTrials.gov). MetS participants (n = 50, 52 ± 10 years) were given dietary instructions and were randomized to 25(OH)VitD 2.000 IU/day p.o. (Suppl group) or no supplementation (No-Suppl group). Serum 25(OH)VitD, oxidized LDL (ox-LDL), paraoxonase activity (PON-1), arylesterase activity (ARYL) and urine 8-isoprostane (8-iso-PGF2a) levels were measured at baseline and after 3 months. Results MetS patients had low baseline 25(OH)VitD levels, which increased by 90% in the Suppl group [from 16.1 (3.3–35.1) to 30.6 (8.4–67.6) ng/mL, p = 0.001] and by 33.3% in the No-Suppl group [from 9.9 (4.0–39.6) to 13.2 (3.5–36.8) ng/mL, p = NS] after intervention. Ox-LDL, PON-1 and ARYL did not change significantly at follow-up in both groups, except for urine 8-iso-PGF2a levels that decreased by 22.7% in the Suppl group [from 48.8 (26.8–137.1) to 37.7 (12.3–99.0) ng/mmol creatinine, p = 0.015] and by 14.4% in No-Suppl group [from 45.8 (16.6–99.3) to 39.2 (13.3–120.1) ng/mmol creatinine, p = NS]. The reduction in 8-iso-PGF2a levels did not differ significantly between the 2 groups. Conclusion The administration of 25(OH)VitD plus dietary intervention in patients with MetS was not associated with meaningful reductions in oxidative stress markers compared with dietary intervention alone.

IntroductionObesity is associated with cardiovascular disease (CVD) risk factors as well as decreased 25(OH) vitamin D serum levels. We aimed to study 25(OH) vitamin D levels in adolescents with obesity compared with normal weight controls in association with CVD risk factors, and the possible effect of vitamin D supplementation.Material and methodsIn a cross-sectional study, 69 obese and 34 normal-weight adolescents were included. In an interventional study 15 adolescents with obesity and vitamin D insufficiency were given 2000 IU vitamin D per os daily for 3 months.ResultsAdolescents with obesity had significantly lower 25(OH) vitamin D levels compared with normal-weight controls (12.0 (3.0–36.0) vs. 34.0 (10.0–69.0) ng/ml, respectively, p < 0.001). In adolescents with obesity, 25(OH) vitamin D was inversely associated with leptin even after adjustment for body mass index (BMI) (r = –0.340, p = 0.009). Conversely, 25(OH) vitamin D was not related with other parameters, such as BMI, blood pressure, lipids, glucose, insulin, homeostasis model assessment (HOMA) index, adiponectin, leptin/adiponectin ratio, and visfatin levels. Following supplementation in 15 vitamin D insufficient adolescents with obesity, 25(OH) vitamin D significantly increased (from 17.3 (12.5–27.8) to 32.6 (14.3–68.0) ng/ml, p = 0.005) and so did low-density lipoprotein cholesterol (LDL-C) (from 85.4 ±9.5 to 92.1 ±15.8 mg/dl, p = 0.022), while there were reductions in glycated haemoglobin (HbA1c) (from 5.8 ±0.2 to 5.5 ±0.1%, p = 0.03) and leptin (from 19.7 (7.8–45.5) to 15.1 (4.3–37.3) ng/ml, p = 0.03). Oxidised LDL, paraoxonase, arylesterase, and urine isoprostanes remained unchanged.ConclusionsAdolescents with obesity had lower 25(OH) vitamin D, which may be associated with higher leptin levels. Vitamin D supplementation may lead to HbA1c and leptin reductions, but also to an increase in LDL-C.

Introduction: Patients with metabolic syndrome (MetS) may have lower 25-hydroxyvitamin D (25(OH)VitD) serum levels compared with non-MetS individuals. Vitamin D (VitD) deficiency is associated with various cardiovascular disease (CVD) risk factors. Yet, the effect of VitD supplementation on MetS remains uncertain. Our aim was to examine the effect of VitD supplementation on CVD risk factors in MetS subjects. Material and methods: This pilot study had a PROBE (prospective, randomised, open-label, blinded end-point) design. Fifty patients with MetS were included and randomised either to dietary instructions (n = 25) (control group) or dietary instructions plus VitD 2000 IU/day (n = 25) (VitD group) for 3 months. This study is registered in ClinicalTrials.gov (NCT01237769). Results: In both groups a similar small weight reduction was achieved. In the VitD group serum 25(OH)VitD levels significantly increased by 91% (from 16.0 (3.0–35.0) to 30.6 (8.4–67.0) ng/ml, p < 0.001), while in the control group no significant change was observed (from 10.0 (4.0–39.6) to 13.0 (3.5–37.0) ng/ml). In both groups triglycerides, high-density lipoprotein cholesterol, low-density lipoprotein cholesterol, fasting glucose, haemoglobin A1c, homeostasis model assessment index and diastolic blood pressure did not significantly change. Systolic blood pressure decreased by 3.7% (from 134 ±14 to 129 ±13 mm Hg, p = 0.05) in the VitD group, while it decreased by 1.5% (from 132 ±13 to 130 ±16 mm Hg, p = NS) in the control group (p = NS between groups). In the VitD group serum 25(OH)VitD increase was negatively correlated with SBP decrease (r = –0.398, p = 0.049). Conclusions: VitD supplementation (2000 IU/day) did not affect various CVD risk factors in patients with MetS.

Background: Patients with metabolic syndrome (MetS) have low serum 25-hydroxyvitamin D (25(OH)VitD) levels. Low 25(OH)VitD has been associated with several emerging cardiovascular disease (CVD) risk factors, while VitD administration may ameliorate them. Aim: To study the effect of 25(OH)VitD supplementation plus dietary instructions on novel CVD risk factors in MetS patients. Methods: This is a pre-specified analysis of a previously published study. Patients with MetS (n = 50, 52 ± 10 years) were given dietary instructions and were randomized to receive either 25(OH)VitD, 2.000 IU/day p.o. (Suppl group) or nothing (No-Suppl group). Serum 25(OH)VitD, small dense low-density lipoprotein cholesterol (sdLDL), as well as lipoprotein-associated phospholipase A2 (LpPLA2) activity, leptin and adiponectin levels were measured at baseline and 3 months later. Results: In the Suppl group 25(OH)VitD levels increased by 90% [from 16.1 (3.3–35.1) to 30.6 (8.4–67.6) ng/mL, p = 0.001] and by 33.3% [from 9.9 (4.0–39.6) to 13.2 (3.5–36.8) ng/mL, p = NS] in the No-Suppl group. sdLDL serum levels, mean LDL size, LpPLA2 activity, leptin, adiponectin concentration and leptin to adiponectin ratio did not change significantly in both groups. Conclusion: In this small study the administration of 25(OH)VitD plus dietary intervention in patients with MetS were not associated with any significant change in various emerging CVD risk factors. (NCT01237769 ClinicalTrials.gov). Keywords: Metabolic syndrome, 25(OH)VitD, Small dense low-density lipoprotein cholesterol, Lipoprotein-associated phospholipase A2, Leptin, Adiponectin

Background: Low levels of 25(OH) vitamin D [25(OH)VitD] have been recognized as a new cardiovascular disease (CVD) risk factor. Statins seem to increase 25(OH)VitD concentration. Aim: To investigate whether combined treatment with the usual dose of rosuvastatin plus fenofibrate or omega-3 fatty acids would increase 25(OH)VitD levels compared with the high-dose rosuvastatin monotherapy in participants with mixed dislipidemia. Methods: We randomly allocated 60 patients with mixed dyslipidemia (low-density lipoprotein cholesterol: >160 mg/dL plus triglycerides: >200 mg/dL) to receive rosuvastatin 40 mg (n = 22), rosuvastatin 10 mg plus fenofibrate 200 mg (n = 21), or rosuvastatin 10 mg plus omega-3 fatty acids 2 g (n = 17) daily for 3 months. Our primary end point was changes in the levels of serum 25(OH)VitD. Results: Rosuvastatin monotherapy was associated with a 53% increase in 25(OH)VitD (from 14.6 [1.0-38.0] to 17.8 [5.3-49.6] ng/mL; P = .000). Rosuvastatin plus micronized fenofibrate and rosuvastatin plus omega-3 fatty acids were associated with increases of 64% (from 14.1 [1.0-48.0] to 18.4 [6.7-52.4] ng/mL, P = .001) and 61% (from 10.4 [6.6-38.4] to 14.0 [9.6-37.6] ng/mL, P = .04), respectively. The changes in 25(OH)VitD after treatment were comparable in the 3 groups. Conclusion: High-dose rosuvastatin monotherapy and the usual dose of rosuvastatin plus fenofibrate or omega-3 fatty acids are associated with significant and similar increases in the 25(OH)VitD levels. This increase may be relevant in terms of CVD risk prevention.

Introduction Several studies implicate an inverse relationship between 25-hydroxy vitamin D (25(OH)Vit D) serum levels and metabolic syndrome (MetS). We sought to investigate a possible relationship between 25(OH)Vit D and emerging risk factors associated with MetS, such as small dense low-density lipoprotein cholesterol (sdLDL-C) concentration, lipoprotein-associated phospholipase A(2) (Lp-PLA(2)) activity and high-sensitivity C-reactive protein (hsCRP) levels. Material and methods We studied 110 consecutive otherwise healthy individuals. Of these, 52 were diagnosed with MetS and 58 who did not meet the MetS criteria served as controls. Low-density lipoprotein (LDL) subclass analysis was performed by polyacrylamide gel electrophoresis. Lp-PLA(2) activity was determined in total plasma by the trichloroacetic acid precipitation procedure. Serum 25(OH)Vit D was determined quantitatively by an enzyme immunoassay method. Results Metabolic syndrome subjects had significantly lower 25(OH)Vit D levels (11.8 [0.6-48.3] ng/ml; 29.5 [1.5-120.75] nmol/l) compared with controls (17.2 [4.8-62.4] ng/ml; 43 [12-156] nmol/l, p = 0.027). Univariate regression analysis showed that 25(OH)Vit D concentration was inversely related to triglycerides (r= - 0.416, p = 0.003) and sdLDL-C (r= - 0.305, p = 0.004). There was no association of 25(OH)Vit D with waist circumference, blood pressure, high-density lipoprotein cholesterol (HDL-C), fasting glucose, Lp-PLA(2) and hsCRP. In multivariate regression analysis the relationship between 25(OH)Vit D and sdLDL-C became insignificant when triglycerides were included in the model. Conclusions Subjects with MetS exhibit lower 25(OH)Vit D serum levels compared with non-MetS individuals. Low 25(OH)Vit D is associated with higher sdLDL-C levels possibly through elevated triglycerides. No association between 25(OH)Vit D and Lp-PLA(2) or hsCRP was found.

Among children and adolescents, metabolic syndrome (MetS) is more common than previously believed. Hence, any information on the relation between vitamin D insufficiency/deficiency and insulin resistance (IR) in this population with risk of developing MetS is of great importance. This review analyzes and evaluates the existing evidence from cross-sectional, observational, and retrospective studies concerning the effect of vitamin D insufficiency/deficiency on MetS as a whole or on its various components. Most data show that insufficient vitamin D status is associated with increased prevalence of MetS or its individual components, mainly blood pressure and IR, often independent of overall obesity or abdominal adiposity. The implications of these findings could be associated with increased risk for developing cardiovascular disease and type 2 diabetes mellitus in later life. The very few randomized control trials examining any possible beneficial effects of vitamin D supplementation are also included.

Backround: Low levels of 25-hydroxyvitamin D (25(OH)VitD) have been recognized as an emerging cardiovascular disease (CVD) risk factor. Statins are reported to increase 25(OH)VitD concentration. Animal studies suggest that ezetimibe is a moderate inhibitor of intestinal 25(OH)VitD absorption, but its effect in humans is unknown. Aim: To investigate whether combined treatment with simvastatin/ezetimibe 10/10 mg would increase 25(OH)VitD levels compared to simvastatin 40 mg monotherapy in patients with primary hypercholesterolemia. Methods: In a Prospective Randomized Open-label Blinded End point study, 50 patients with primary hypercholesterolemia received either simvastatin/ezetimibe 10/10 mg (n = 25) or simvastatin 40 mg (n = 25) daily for 3 months. The primary end point was between-group difference in the change of serum 25(OH)VitD levels. Results: Simvastatin/ezetimibe 10/10 mg was associated with a 36.7% increase in 25(OH)VitD serum levels (from 6.8 to 9.3 ng/mL, P = .000), while simvastatin 40 mg was associated with a 79.1% increase (from 6.7 to 12.0 ng/mL, P = .008). The increase in 25(OH)VitD levels in the simvastatin 40 mg group was significantly greater compared to that in the simvastatin/ezetimibe 10/10 mg group ( P = .04). Both groups exhibited similar reductions in low-density lipoprotein cholesterol (LDL-C) levels. Conclusion: For similar LDL-C lowering simvastatin 40 mg is associated with greater increase in 25(OH)VitD compared to simvastatin/ezetimibe 10/10 mg. Whether this difference is relevant in terms of CVD risk reduction is unknown.

Vitamin D is a steroid molecule, mainly produced in the skin that regulates the expression of a large number of genes. Until recently its main known role was to control bone metabolism and calcium and phosphorus homeostasis. During the last 2 decades it has been realized that vitamin D deficiency, which is really common worldwide, could be a new risk factor for many chronic diseases, such as the metabolic syndrome and its components, the whole spectrum of cardiovascular diseases, several auto-immune conditions, and many types of cancer as well as all-cause mortality. Except for the great number of epidemiological studies that support the above presumptions, vitamin D receptors (VDRs) have been identified in many tissues and cells. The effect of vitamin D supplementation remains controversial and the need for more persuasive study outcomes is intense.