Correcting vitamin D insufficiency improves insulin sensitivity in obese adolescents: a randomized controlled trial.
What this study found
Vitamin D3 supplementation safely corrected insufficiency in most participants and improved markers of insulin sensitivity compared with placebo. By 6 months, 93% of the vitamin D group had sufficient 25(OH)D, and between-group changes favored vitamin D for fasting insulin (P = 0.026), HOMA-IR (P = 0.033), QUICKI (P = 0.016), and leptin-to-adiponectin ratio (P = 0.045). Fasting glucose did not show a significant between-group change (P = 0.085), and CRP, IL-6, and TNF-alpha were largely unchanged. The authors concluded that correcting vitamin D insufficiency may be a useful adjunct to…
- Study & population
- Randomized controlled trial in obese adolescents with baseline vitamin D deficiency or insufficiency.
- Intervention
- Vitamin D3 (cholecalciferol) 4000 IU/day was given orally as two indistinguishable 2000 IU pills daily for 6 months.
- Key limitation
- The trial was small, with only 21 participants in the vitamin D arm and 23 in placebo, which limits precision.
View source
Open PDFOriginal abstract
BACKGROUND Obese adolescents are at a greater risk of vitamin D deficiency because vitamin D is thought to be sequestered by excess adipose tissue. Poor vitamin D status has been associated with a higher prevalence of the metabolic syndrome, type 2 diabetes, or both in adults and adolescents. OBJECTIVE The objective was to determine in obese adolescents the efficacy and safety of 4000 IU vitamin D3/d and whether subsequent increased circulating concentrations of 25-hydroxyvitamin D [25(OH)D] are associated with improved markers of insulin sensitivity and resistance and reduced inflammation. DESIGN Obese adolescent patients [n = 35; mean ± SD age: 14.1 ± 2.8 y; BMI (in kg/m(2)): 39.8 ± 6.1; 25(OH)D: 19.6 ± 7.1 ng/mL] were recruited from the University of Missouri Adolescent Diabetes and Obesity Clinic and were randomly assigned to receive either vitamin D3 (4000 IU/d) or placebo as part of their standard care. Anthropometric measurements, inflammatory markers (IL-6, TNF-α, C-reactive protein), adipokines (leptin, adiponectin), fasting glucose, fasting insulin, and HOMA-IR values were measured at baseline and at 2 follow-up visits (3 and 6 mo). RESULTS After 6 mo, there were no significant differences in BMI, serum inflammatory markers, or plasma glucose concentrations between groups. Participants supplemented with vitamin D3 had increases in serum 25(OH)D concentrations (19.5 compared with 2.8 ng/mL for placebo; P < 0.001), fasting insulin (-6.5 compared with +1.2 μU/mL for placebo; P = 0.026), HOMA-IR (-1.363 compared with +0.27 for placebo; P = 0.033), and leptin-to-adiponectin ratio (-1.41 compared with +0.10 for placebo; P = 0.045). Inflammatory markers remained unchanged. CONCLUSION The correction of poor vitamin D status through dietary supplementation may be an effective addition to the standard treatment of obesity and its associated insulin resistance. This trial was registered at clinicaltrials.gov as NCT00994396.