cholecalciferol and Dyslipidemias

Evidence of synergic health effects of co-supplementation with vitamin D and probiotics is emerging. Following the Preferred Reporting Items for Systematic Reviews and Meta-Analyses PRISMA statement, scientific databases and the grey literature were searched, and a narrative review and risk of bias assessment were conducted. Seven randomized controlled trials were included, which had low risk of bias. Six studies were double-blind, and once single-blind, extended over 6-12 weeks, and included 50-105 participants. Conditions explored included schizophrenia, gestational diabetes, type 2 diabetes and coronary heart disease, polycystic ovarian syndrome, osteopenia, irritable bowel syndrome (IBS), and infantile colic. Supplementation frequency was daily or bi-monthly, with mainly vitamin D3, and

Topics: Bifidobacterium; Cholecalciferol; Dietary Supplements; Dyslipidemias; Female; Humans; Inflammation; Insulin Resistance; Lactobacillus; Male; Mental Health; Probiotics; Randomized Controlled Trials as Topic; Streptococcus

Atherosclerosis is common in patients with chronic kidney disease (CKD), and cardiovascular disease (CVD) represents a major cause of death in these patients, especially, in patients with end-stage renal disease(ESRD). The pathological features in ESRD patients are intimal atherosclerosis and medial calcific sclerosis. The important risk factors for CVD in ESRD patients are hypertension, dyslipidemia and CKD bone and mineral disorder (CKD-MBD). Atherosclerosis has been evaluated by measurements of intima-media thickness and pulse-wave velocity. Although the target blood pressure still undetermined, hypertension would be treated with renin-angiotensin system inhibitors. In addition, treatment of dyslipidemia with statins may lead to favorable CVD outcome. Finally, inhibition of vascular calcification should be important by treatment with active vitamin D and sevelamer.

Topics: Angiotensin Receptor Antagonists; Angiotensin-Converting Enzyme Inhibitors; Atherosclerosis; Bone Diseases, Metabolic; Calcinosis; Cholecalciferol; Chronic Disease; Dyslipidemias; Humans; Hydroxymethylglutaryl-CoA Reductase Inhibitors; Hypertension; Kidney Failure, Chronic; Polyamines; Risk Factors; Sevelamer; Tunica Intima; Vascular Diseases

Low vitamin D serum levels have been associated with unfavourable lipid profile and poorer response to atorvastatin. Aims of this study were to test the effects of 25-hydroxyvitamin D3 (calcifediol) compared to parental vitamin D3 (cholecalciferol) supplementation on modifications of plasma 25(OH)D levels and lipid profile.. Fifty-seven postmenopausal women (aged 59.03 ± 6.73 years) who were at low risk of fracture and with basal plasma 25(OH)D < 30 ng/mL were included if they were on atorvastatin treatment prescribed as appropriate. Recruited women were randomized to receive oral calcifediol or cholecalciferol, both at a dose of 140 μg according to a weekly regimen.. At baseline, 25(OH)D was negatively associated with BMI (r = -0.37; P = 0.004), total cholesterol (r = -0.31; P = 0.01) and LDL-C (r = -0.32; P = 0.02). After 24 weeks, 25(OH)D increased significantly in both groups (P < 0.001), although higher levels were obtained with calcifediol as compared with cholecalciferol (P < 0.001). Only in the calcifediol group, a significant reduction of LDL-C (P = 0.01) and an increase of HDL-C (P = 0.02) were obtained, even after adjustment for age, and baseline BMI, 25(OH)D and lipid levels (P < 0.05). The percentage changes in 25(OH)D levels were associated with the variations of LDL-C (r = -0.44; P = 0.01) and HDL-C levels (r = 0.30; P = 0.10).. Calcifediol administration in osteopenic and dyslipidemic postmenopausal women with low 25(OH)D improves lipid profile when added to an ongoing atorvastatin treatment.

Topics: Administration, Oral; Atorvastatin; Bone Diseases, Metabolic; Calcifediol; Cholecalciferol; Dietary Supplements; Drug Therapy, Combination; Dyslipidemias; Female; Heptanoic Acids; Humans; Hydroxymethylglutaryl-CoA Reductase Inhibitors; Lipid Metabolism; Middle Aged; Postmenopause; Pyrroles; Vitamin D; Vitamin D Deficiency; Vitamins

Dyslipidemia is a lifestyle-related (physical inactivity or obesity) disease; therefore, dietary foods that can easily be consumed in daily life is important to prevent dyslipidemia. Ergosterol, a precursor of vitamin D

Topics: Animals; Biosynthetic Pathways; Cholecalciferol; Cholesterol; Diet; Diet, High-Fat; Dyslipidemias; Ergosterol; Humans; Rats; Sucrose; Vitamin D; Vitamins

Epidemiological outburst of type 2 diabetes is of great global concern. T2D starts with Insulin Resistance (IR) which arises largely due to environmental factors and to a lesser extent due to genetic factor. IR gradually develops into T2D and encompasses a wide array of conditions including Impaired Glucose Tolerance (IGT), hyperinsulinemia, Impaired Fasting Glucose (IFG), and Impaired Insulin Release (IIR). Initiation of IR increases the risk of Cardiovascular Diseases (CVD). Therefore, early diagnosis and management of IR and its related outcomes (hyperinsulinemia, hyperglycemia, and dyslipidemia) should be the prime focus of intervention therapies. Present research aimed to evaluate the synergistic combination of Magnesium orotate (MOD), Menaquinone- 7 (MK-7), and Cholecalciferol (CHOL) for the management of these therapeutic targets in the Streptozotocin-Nicotinamide-induced T2D Wistar rat model. Synergistic combination was found to be superior over its individual components in management of hyperglycemia, impaired insulin secretion, Homeostatic Model Assessment of Insulin Resistance (HOMA-IR), and dyslipidemia (p < 0.01 or p < 0.05). Its effect was found to be equivalent or better than reference drugs (p < 0.01 or p < 0.05). Histopathological analysis depicted that combination treatment was able to regenerate and preserve pancreatic β-cell mass in diabetic rats. In conclusion, combination studied in present research can be evaluated further under clinical settings for management of IR and its related outcomes.

Topics: Animals; Cholecalciferol; Diabetes Mellitus, Experimental; Disease Models, Animal; Dyslipidemias; Hypoglycemic Agents; Male; Niacinamide; Orotic Acid; Rats; Rats, Wistar; Streptozocin; Vitamin K 2

Recent studies have highlighted a significant association between the severity of atherosclerosis and bone mineral density (BMD) among healthy subjects, although its connection to angiographically determined peripheral artery disease (PAD) has never been investigated. We evaluated the connection between the angiographic severity and site specificity of peripheral atherosclerosis and osteoporosis among patients with chronic lower limb ischemia. In our cross-sectional study we investigated 172 patients with PAD. The anatomic sites of the lesions were analyzed. The severity of atherosclerosis was diagnosed using the Bollinger angiographic score (BS). BMD was measured at the lumbar spine (l-BMD) and at femoral (f-BMD) and radial (r-BMD) sites by dual-energy X-ray absorptiometry. Dyslipidemia, the level of vitamin D(3), and different bone turnover markers were also noted. Among PAD patients, regardless of the lesion site, we did not find any association between BMD and BS. Among patients with iliac disease, BS was associated with l-BMD (p = 0.038, r = -0.467) and with f-BMD (p = 0.002, r = -0.642). The level of r-BMD among patients with iliac disease was not associated with BS (p = 0.233, r = -0.306). We did not find any difference between the group of patients with and that without dyslipidemia and low or normal levels of vitamin D(3). Our results show a connection between the severity of atherosclerosis and osteoporosis among patients with PAD, specific to the site of the lesion. The findings regarding dyslipidemia, bone markers, and site specificity support the hypothesis that reduced blood flow is the key factor responsible for the inverse association of BMD with atherosclerosis.

Topics: Absorptiometry, Photon; Aged; Atherosclerosis; Bone Density; Cholecalciferol; Cross-Sectional Studies; Dyslipidemias; Female; Humans; Male; Middle Aged; Osteoporosis; Peripheral Arterial Disease