• Kaplan-Meier estimate
• NHANES
• cox proportional hazards analysis
• homocysteine
• hyperlipidemia

• cardiovascular prevention
• cholesterol
• dyslipidemia
• triglycerides
• vitamin D

• Humans
• Dyslipidemias/blood
• Vitamin D/blood
• Vitamin D Deficiency/complications
• Vitamin D Deficiency/blood
• Cardiovascular Diseases/prevention & control
• Cardiovascular Diseases/etiology
• Lipids/blood

• 25-hydroxyvitamin D
• insulin resistance
• metabolic-associated fatty liver disease
• triglyceride-glucose index

• the key project of Wuhan Municipal Health Commission

• Humans
• Fatty Acids, Omega-3/adverse effects
• Cholecalciferol
• Lipoproteins, LDL
• Cholesterol
• Vitamin D Deficiency/diagnosis
• Vitamin D Deficiency/drug therapy

Insulin resistance increases the risk of developing diabetes, and the degree of resistance influences the glycemic control of patients with diabetes. Numerous researchers have focused on improving insulin sensitivity in order to prevent diabetes-related complications and other chronic diseases. Several studies have also linked vitamin D levels to insulin secretion and resistance, given that both vitamin D and its receptor complex play important roles in regulating pancreatic β-cells. It has been suggested that vitamin D supplementation improves vitamin D levels, but further research is needed to confirm this as neither insulin function nor glycemic control improves when vitamin D levels increase. Magnesium is a cofactor for many enzymes. Although the role of magnesium in the management of diabetes has long been evaluated, it has not yet been determined whether magnesium supplements improve insulin function. However, several researchers have found that patients with good glycemic control have high magnesium levels. Magnesium is closely related to vitamin D and is necessary for the transport and activation of vitamin D in humans. Combined supplementation with vitamin D and magnesium improves glycemic control in patients with diabetes.

• Vitamin D
• Magnesium
• Diabetes
• Insulin sensitivity
• Insulin resistance
• Glycemic control

• Cardiac-metabolic
• Elderly
• Supplementation
• Vitamin D

• C-Tn
• C-terminal pro-endothelin-1
• HFABP
• Myocardial injury
• vitamin D3

• Animals
• Atorvastatin/pharmacology
• Atorvastatin/therapeutic use
• Biomarkers
• Cholecalciferol/pharmacology
• Diabetes Mellitus
• Rats
• Rats, Wistar

• 25(OH)D
• BRIEF-A
• CRP
• HbA1c
• IL-6
• T2DM
• sTREM1

• Adult
• Humans
• Diabetes Mellitus, Type 2/metabolism
• Glycated Hemoglobin
• Interleukin-6/metabolism
• Blood Glucose/analysis
• Cognitive Dysfunction/complications
• Lipid Metabolism
• Glycolipids

• National Natural Science Foundation of China

• elastography
• non-alcoholic fatty liver disease
• treatment
• vitamin D

• Adult
• Elasticity Imaging Techniques
• Humans
• Liver/diagnostic imaging
• Liver/pathology
• Liver Cirrhosis/diagnostic imaging
• Liver Cirrhosis/drug therapy
• Liver Cirrhosis/pathology
• Non-alcoholic Fatty Liver Disease/complications
• Non-alcoholic Fatty Liver Disease/diagnostic imaging
• Non-alcoholic Fatty Liver Disease/drug therapy
• Uric Acid
• Vitamin D

• The authors declare that there was no financial support for this study.

• 25-hydroxyvitamin D
• diabetes mellitus
• glycated hemoglobin
• type 2

• not being supported by a grant

Background: Due to inconsistent evidence regarding the potential role of vitamin D on lipid profile and sirtuin 1 (SIRT-1), this study was designed to investigate the effect of vitamin D supplementation in combination with weight loss diet on lipid profile and SIRT-1 in obese subjects with vitamin D deficiency.

Methods: Forty-four obese subjects with vitamin D deficiency were randomly assigned in a randomized clinical trial to receive either a weight reduction diet supplemented with 50000IU vitamin D3 pearl (n = 22) or placebo (n = 22) once weekly for 12 weeks. Changes in total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), triglyceride (TG) and low high density lipoprotein cholesterol (HDL-C) and SIRT-1 were the primary outcomes. Secondary outcomes were changes in body mass index (BMI), 25(OH) D and parathyroid hormone (PTH). Physical activity and dietary intakes were also assessed.

Results: During the intervention, PTH (mean difference, -33.36; 95% CI: -49.15 to -17.57;P<0.001) and LDL-C (mean difference, -15.91; 95% CI: -21.76 to -10.07; P<0.001) decreased and 25(OH) D (mean difference, 36.44; 95% CI: 29.05 to 43.83; P<0.001) increased significantly in the vitamin D group. BMI (mean differences: -2.40; 95% CI: [-2.92 to-1.88] in vitamin D group and mean differences: -1.90; 95% CI [-6.58 to -3.01] in placebo group, P<0.05 for both groups), TC (mean difference,-21.31; 95% CI: -27.24 to -15.38; P<0.001 in vitamin D group and mean difference, -12.54; 95% CI: -19.02 to -6.06; P<0.001 in placebo group) and TG (mean difference,-21.31; 95% CI: -27.24 to -15.38; P<0.001in vitamin D group and mean difference, -12.54; 95% CI: -19.02 to -6.06; P<0.001 in placebo group) decreased and SIRT-1(mean difference, 3.95; 95% CI: 1.18 to 6.73; P=0.007in vitamin D group and mean difference,1.91; 95% CI: 0.31 to 3.63 in placebo group, P=0.022) increase significantly in both group. At end of the study, 25(OH) D and PTH showed significant differences in between-group analyses(P<0.05). No significant difference was detected for HDL-C in within and between groups.

Conclusion: This study gives no support for any beneficial effect of vitamin D supplementation on lipid profile and SIRT-1 in obese subjects with vitamin D deficiency.

• Lipid profile
• Obesity
• Sirtuin1
• Vitamin D
• Weight loss diet

• Inflammation
• NAFLD
• Obesity
• Oxidative stress
• Vitamin D

• Dietary Supplements
• Humans
• Non-alcoholic Fatty Liver Disease/etiology
• Non-alcoholic Fatty Liver Disease/prevention & control
• Prognosis
• Risk Factors
• Severity of Illness Index
• Vitamin D/administration & dosage
• Vitamin D Deficiency/complications
• Vitamins/administration & dosage

To evaluate the association between the level of vitamin D and glycemic control among patients with diabetes.

We analyzed data collected from NHANES 2003–2006. We included only non-pregnant adult diabetic persons 18 years or older. Participants who had vitamin D level less than 20 ng/ml were considered as having vitamin D deficiency. Participants were considered to have a glucose control if the HbA_1c level was less than 7% [53 mmol/L]. We used student’s t test to compare the difference in HbA_1c means between people with Diabetes with and without a vitamin D deficiency. We used a multivariate logistic regression model to predict the relationship between glucose control and vitamin D deficiency. We used race/ethnicity, BMI, age, gender, type of diabetic medication used, having health insurance or not, and comorbid conditions (hypertension, anemia, cholesterol, liver disease, and kidney disease) as control variables.

The study population included a total of 929 non-institutionalized, non-pregnant, diabetic adult persons. About 57% of patients with diabetes had a vitamin D deficiency. Blacks (non-Hispanic patients) with diabetes had the highest rate of vitamin D deficiency (79%). The unadjusted means of HbA_1c were significantly different between diabetic patients with no vitamin D deficiency and those with a vitamin D deficiency (7.06% [54 mmol/L], 7.56 % [59 mmol/L], respectively, P < 0.0001). Multivariate adjustment showed a small but not significant, increase in odds (11%) of having uncontrolled diabetes in patients with a vitamin D deficiency after adjustment for other factors.

Vitamin D deficiency is very common in patients with diabetes. We found no significant association between vitamin D level and glycemic control in patients with diabetes after adjustment for control variables.

• Diabetes
• Glucose control
• HbA1c
• Vitamin D deficiency

• Dietary Supplements
• Female
• Humans
• Insulin Resistance
• Lipoproteins, VLDL/blood
• Polycystic Ovary Syndrome/blood
• Polycystic Ovary Syndrome/drug therapy
• Vitamin D/administration & dosage

• muscle strength
• osteoarthritis
• physical performance
• vitamin D2 supplementation

• Aged
• Biomarkers/blood
• Biomechanical Phenomena
• Body Composition/drug effects
• Dietary Supplements
• Ergocalciferols/therapeutic use
• Female
• Hand Strength
• Health Status
• Humans
• Knee Joint/diagnostic imaging
• Knee Joint/drug effects
• Knee Joint/physiopathology
• Male
• Middle Aged
• Muscle Strength/drug effects
• Osteoarthritis, Knee/diagnosis
• Osteoarthritis, Knee/drug therapy
• Osteoarthritis, Knee/physiopathology
• Osteoarthritis, Knee/psychology
• Oxidative Stress/drug effects
• Pain Measurement
• Protein Carbonylation/drug effects
• Quality of Life
• Recovery of Function
• Thailand
• Time Factors
• Treatment Outcome
• Vitamin D/analogs & derivatives
• Vitamin D/blood
• Vitamin D Deficiency/blood
• Vitamin D Deficiency/diagnosis
• Vitamin D Deficiency/drug therapy

The aim of the current trial was to investigate the effect of Vitamin D treatment on metabolic markers in people with Vitamin D deficiency and thyroid autoimmunity.

In this double-blind, randomized, placebo-controlled clinical trial, 65 Vitamin D deficient euthyroid or hypothyroid patients with positive TPO-Ab were enrolled. They randomly allocated into two groups to receive oral Vitamin D_{3 (}50000 IU weekly) and placebo for 12 weeks. Serum concentration of calcium, phosphorus, albumin, C-reactive protein, blood urea nitrogen, creatinine, glycated hemoglobin (HbA1c), insulin, fasting plasma glucose (FPG), triglyceride (TG), total cholesterol, and high-density lipoprotein were measured in both groups before and after the trial. Homeostasis model assessment estimates of beta cell function (HOMA-B) and HOMA-insulin resistance (HOMA-IR) were calculated before and after trial in both groups.

Thirty-three and thirty-two participants were allocated to Vitamin D-treated and placebo-treated groups, respectively. Mean (standard error) level of Vitamin D increased significantly in Vitamin D-treated group (45.53 [1.84] ng/mL vs. 12.76 [0.74] ng/mL, P = 0.001). The mean of HbA1c and insulin was increased significantly both in Vitamin D-treated and placebo-treated groups (P < 0.05). Other variables did not meet a significant change after trial (P = NS). In between-group comparison, there was not any significant difference between Vitamin D-treated and placebo-treated groups regarding measures of HOMA-B, HOMA-IR, FPG, HbA1c, and TG (P = NS).

Our findings showed that weekly 50000 IU oral Vitamin D3 for 12 weeks did not improve metabolic markers, IR, or insulin secretion in Vitamin D deficient patients with Hashimoto thyroiditis.

• Fasting plasma glucose
• Hashimoto disease
• Vitamin D deficiency
• insulin resistance
• insulin secretion
• lipids