Table 2.

Effects of vitamin D supplementation on β-cell function, insulin sensitivity, and adipokines related to energy homeostasis in humans.

Participants	Type of Vitamin D, Dose, Duration	Results
96 participants with prediabetes or with newly diagnosed type 2 diabetes [39]	Vitamin D3, 5000 IU/day vs. placebo, 6 months	- Increased M-value (a marker of peripheral insulin sensitivity) in the vitamin D group vs. stable in the placebo group (p = 0.009) - Improved β-cell function (disposition index) in the vitamin D group vs. stable in the placebo group (p = 0.039)
20 participants with type 2 diabetes [40]	Vitamin D3, 5000 IU/day vs. placebo, 12 weeks	- Increased HOMA-%B in the vitamin D group (p = 0.03) * vs. non-significant increased HOMA-%B in the placebo group (p = 0.08) *
56 women with gestational diabetes (at 24–28 weeks of gestation) [41]	Vitamin D3 50,000 IU at baseline and day 21 + calcium 1000 mg/day vs. placebo, 3 weeks	- Decreased HOMA-IR in the treatment group vs. stable in the placebo group (p = 0.001) - Increased QUICKI in the treatment group vs. stable in the placebo group (p = 0.003) - A significant increase in GSH in the treatment group when compared with the placebo group (p = 0.03) - A smaller increase in MDA in the treatment when compared with the placebo group (p = 0.03)
54 participants with obesity and vitamin D deficiency (25(OH)D < 20 ng/mL) [43]	Vitamin D3 100,000 IU bolus, then 4000 IU/day vs. placebo, 16 weeks	- Greater increases in adiponectin (p = 0.002) and leptin (p = 0.002) in the vitamin D group when compared with the placebo group a

25(OH)D: 25-hydroxyvitamin D; GSH: glutathione; HOMA-% B: homeostasis model of assessment of β-cell activity; HOMA-IR: homeostasis model of assessment for insulin resistance; MDA: malondialdehyde: QUICKI: quantitative insulin sensitivity check index; *, different within group; ^a, after adjustment for baseline 25(OH)D levels, season, sun exposure, and dietary vitamin D intake.