Vitamin D, Insulin Secretion, Sensitivity, and Lipids
What this study found
Vitamin D3 supplementation raised serum 25(OH)D and lowered PTH, but it did not improve insulin secretion, insulin sensitivity, or lipid profile versus placebo after 6 months. Mean serum 25(OH)D reached 142.7 nmol/L in the vitamin D group versus 42.9 nmol/L in placebo, with no statistically significant between-group differences in the metabolic outcomes. Compliance was high at 98% in the vitamin D group and 97% in placebo. No cases of hypercalcemia or kidney stones were observed.
- Study & population
- Randomized, double-blind, placebo-controlled trial nested in the population-based Tromsø Study in Norway.
- Intervention
- Vitamin D3 was given as 20,000 IU per capsule by mouth twice per week for 6 months, using a placebo-controlled double-blind design.
- Key limitation
- The intervention arm was small, with only 49 completers, and follow-up lasted just 6 months, limiting power to detect modest metabolic effects.
Original abstract
OBJECTIVE Vitamin D deficiency is associated with an unfavorable metabolic profile in observational studies. The intention was to compare insulin sensitivity (the primary end point) and secretion and lipids in subjects with low and high serum 25(OH)D (25-hydroxyvitamin D) levels and to assess the effect of vitamin D supplementation on the same outcomes among the participants with low serum 25(OH)D levels. RESEARCH DESIGN AND METHODS Participants were recruited from a population-based study (the Tromsø Study) based on their serum 25(OH)D measurements. A 3-h hyperglycemic clamp was performed, and the participants with low serum 25(OH)D levels were thereafter randomized to receive capsules of 20,000 IU vitamin D3 or identical-looking placebo twice weekly for 6 months. A final hyperglycemic clamp was then performed. RESULTS The 52 participants with high serum 25(OH)D levels (85.6 ± 13.5 nmol/L [mean ± SD]) had significantly higher insulin sensitivity index (ISI) and lower HbA1c and triglycerides (TGs) than the 108 participants with low serum 25(OH)D (40.3 ± 12.8 nmol/L), but the differences in ISI and TGs were not significant after adjustments. After supplementation, serum 25(OH)D was 142.7 ± 25.7 and 42.9 ± 17.3 nmol/L in 49 of 51 completing participants randomized to vitamin D and 45 of 53 randomized to placebo, respectively. At the end of the study, there were no statistically significant differences in the outcome variables between the two groups. CONCLUSIONS Vitamin D supplementation to apparently healthy subjects with insufficient serum 25(OH)D levels does not improve insulin sensitivity or secretion or serum lipid profile.