cholecalciferol and Glucose-Intolerance

There has been conflicting evidence regarding the potential role of vitamin D in glucose homeostasis. This study was designed to investigate the effect of high-dose vitamin D3 treatment on β-cell function, insulin sensitivity, and glucose tolerance in subjects with prediabetes or diet-treated type 2 diabetes.. Subjects (n = 44) were randomized to 30,000 IU vitamin D3 once weekly or placebo for 8 weeks. Hyperglycemic clamp assessed first-phase (0-12 min) and second-phase (12-120 min) insulin response, insulin sensitivity, and disposition index (DI). An oral glucose tolerance test assessed glucose tolerance and glycosylated hemoglobin assessed glycemic control.. A total of 21 (vitamin D) and 22 (placebo) subjects completed the study, respectively. Season-adjusted 25-OH-vitamin D [25(OH)D] levels were doubled in the active treated group (43-82 nmol/L). No effect of vitamin D treatment, compared with placebo, was seen on first-phase or second-phase insulin secretion. There were no group differences in insulin sensitivity, DI, or any measures of glycemic control. No hypercalcemia or other adverse effects of vitamin D treatment were seen compared with placebo. Subgroup analyses of those with the lowest basal and greatest increase in 25(OH)D levels did not change these results.. This study gives no support for any substantial effect of high-dose vitamin D treatment for 8 weeks in prediabetes or diet-treated type 2 diabetes on β-cell function, insulin sensitivity, or glycemic control.

Topics: Aged; Blood Glucose; Cholecalciferol; Diabetes Mellitus, Type 2; Female; Glucose Intolerance; Glucose Tolerance Test; Glycated Hemoglobin; Homeostasis; Humans; Insulin Resistance; Insulin-Secreting Cells; Male; Middle Aged; Prediabetic State; Vitamins

In observational studies, low serum 25-hydroxyvitamin D [25(OH)D] concentrations have been associated with insulin resistance and other risk factors for cardiovascular disease.. We present 1-year data from an ongoing 5-year trial in 511 individuals with impaired fasting glucose (IFG) and/or impaired glucose tolerance (IGT) randomly assigned to 20,000 IU/week vitamin D3 or placebo. An oral glucose tolerance test was performed at baseline and after 1 year.. Mean baseline serum 25(OH)D was 59.9 nmol/L and 61.1 nmol/L in the vitamin D and placebo groups, respectively, and increased by 45.8 nmol/L and 3.4 nmol/L, respectively. With adjustment for baseline concentrations, no differences in measures of glucose metabolism, insulin secretion or sensitivity, blood pressure, or hs-CRP were found after 1 year. There was a slight, but significant decrease in total and LDL cholesterol in the vitamin D group compared with the placebo group, but as there was also a decrease in HDL cholesterol, the change in the total/HDL cholesterol ratio did not differ significantly. Only analyzing subjects with 25(OH)D <50 nmol/L did not change the results.. This study shows that vitamin D supplementation does not improve glycemic indices, blood pressure, or lipid status in subjects with IFG and/or IGT.

Topics: 25-Hydroxyvitamin D 2; Adult; Aged; Aged, 80 and over; Blood Pressure; Calcifediol; Cholecalciferol; Diabetes Mellitus, Type 2; Diabetic Angiopathies; Dietary Supplements; Double-Blind Method; Female; Glucose Intolerance; Glucose Tolerance Test; Humans; Insulin; Insulin Resistance; Lipids; Male; Middle Aged; Prediabetic State; Risk Factors; Vitamin D; Vitamin D Deficiency; Vitamins; Young Adult

Topics: Aged; Aged, 80 and over; Aging; Calcium; Cholecalciferol; Diabetes Mellitus, Type 2; Drug Therapy, Combination; Female; Fractures, Spontaneous; Glucose Intolerance; Humans; Male; Metabolic Syndrome; Osteoporosis; Placebos; Risk Factors; Vitamin D Deficiency; Vitamins

Previous studies have shown that vitamin D3 (VD3) may be a protective factor for diabetes mellitus (DM), while triglycerides/high-density lipoprotein (TG/HDL) may be a risk factor for diabetes. However, no existing study has elucidated the interaction between TG/HDL and VD3. Therefore, this work aimed to investigate the relationships of TG/HDL with insulin resistance (IR), impaired glucose tolerance (IGT), and DM at different VD3 levels.. With the use of the data from five National Health and Nutrition Examination Survey (NHANES) cycles, a total of 2,929 males and 3,031 females were divided into 4 groups according to their VD3 levels. Logistic regression was performed to observe the associations of TG/HDL ratio with IR, IGT, and DM in different groups.. The relationships of TG/HDL with IR, IGT, and DM showed a threshold effect, with the cutoff values of 1.094, 1.51, and 1.11, respectively. On both sides of the cutoff values, the correlation was first weakened and then enhanced with the increase in VD3 levels.. TG/HDL is a risk factor for IR, IGT, and DM. Both too low and too high levels of VD3 can strengthen this association, whereas keeping VD3 at a reasonable level helps to reduce the associations of TG/HDL with IR, IGT, and DM.

Topics: Biomarkers; Cholecalciferol; Cholesterol, HDL; Diabetes Mellitus; Female; Glucose Intolerance; Humans; Insulin Resistance; Lipoproteins, HDL; Male; Nutrition Surveys; Triglycerides

Cholecalciferol (D3) may improve inflammation, and thus provide protection from cardiometabolic diseases (CMD), although controversy remains. Omega-3 fatty acids (ω-3FA) may also prevent the development of CMD, but the combined effects of ω-3FA and D3 are not fully understood.. We determined the chronic independent and combined effects of D3 and ω-3FA on body weight, glucose homeostasis, and markers of inflammation in obese mice.. We gave 8-week-old male C57BL/6J mice, which had been fed a high-fat, high-sucrose (HF) diet (65.5% kcal fat, 19.8% kcal carbohydrate, and 14% kcal protein) for 12 weeks, either a standard D3 dose (+SD3; 1400 IU D3/kg diet) or a high D3 dose (+HD3; 15,000 IU D3/kg diet). We fed 1 +SD3 group and 1 +HD3 group with 4.36% (w/w) fish oil (+ω-3FA; 44% eicosapentaenoic acid, 25% docosahexaenoic acid), and fed the other 2 groups with corn oil [+omega-6 fatty acids (ω-6FA)]. A fifth group was fed a low-fat (LF; 15.5% kcal) diet. LF and HF+ω-6+SD3 differences were tested by a Student's t-test and HF treatment differences were tested by a 2-way ANOVA.. D3 supplementation in the +HD3 groups did not significantly increase plasma total 25-hydroxyvitamin D and 25-hydroxyvitamin D3 [25(OH)D3] versus the +SD3 groups, but it increased 3-epi-25-hydroxyvitamin D3 levels by 3.4 ng/mL in the HF+ω-6+HD3 group and 4.0 ng/mL in the HF+ω-3+HD3 group, representing 30% and 70%, respectively, of the total 25(OH)D3 increase. Energy expenditure increased in those mice fed diets +ω-3FA, by 3.9% in the HF+ω-3+SD3 group and 7.4% in the HF+ω-3+HD3 group, but it did not translate into lower body weight. The glucose tolerance curves of the HF+ω-3+SD3 and HF+ω-3+HD3 groups were improved by 11% and 17%, respectively, as compared to the respective +ω-6FA groups. D3 supplementation, within the ω-3FA groups, altered the gut microbiota by increasing the abundance of S24-7 and Lachnospiraceae taxa compared to the standard dose, while within the ω-6FA groups, D3 supplementation did not modulate specific taxa.. Overall, D3 supplementation does not prevent CMD or enhance the beneficial effects of ω-3FA in vitamin D-sufficient obese mice.

Topics: Animals; Cholecalciferol; Diet, High-Fat; Dietary Sucrose; Dietary Supplements; Drug Synergism; Fatty Acids, Omega-3; Glucose Intolerance; Humans; Leptin; Liver; Male; Metabolic Syndrome; Mice; Mice, Inbred C57BL; Mice, Obese; Obesity; Random Allocation