Correcting vitamin D insufficiency improves insulin sensitivity in obese adolescents: a randomized controlled trial1,2,3
Am J Clin Nutr April 2013 ajcn.050013
Anthony M Belenchia,
Aneesh K Tosh,
Laura S Hillman, and
Catherine A Peterson
1From the Department of Nutrition and Exercise Physiology (AMB and CAP), and the Department of Child Health, University of Missouri School of Medicine (AKT and LSH), University of Missouri, Columbia, MO.
↵2 Supported by a JR Albert Foundation grant (Naperville, IL).
↵3 Address correspondence to CA Peterson, University of Missouri, Department of Nutrition and Exercise Physiology, 217 Gwynn Hall, Columbia, MO 65211. E-mail: petersonca at missouri.edu.
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/m2): 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.
Received September 5, 2012. Accepted January 7, 2013.
A drop of fasting insulin of 6.5μU/mL is huge. The entire range is only 10-25μU/mL
See also VitaminDWiki
- Overview Diabetes and vitamin D
- 2000 IU of vitamin D helped Type 2 diabetic women, but was not enough – July 2012
- Scientific explanation of vitamin D relationship to insulin resistance– Dec 2012
- How often might 50,000 IU vitamin D be taken - results of clinical trials just one capsule every 12 days according to one diabetes RCT
- 4000 IU RCT reduces type 2 diabetes HOMA by 24% and CRP by 64% April 2010 a previous RCT with good results