title: Correcting vitamin D insufficiency improves insulin sensitivity in obese adolescents: a randomized controlled trial.
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.
  
  
  METHODS
  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.
  
  
  CONCLUSIONS
  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.
authors: Department of Nutrition and Exercise Physiology, University of Missouri, Columbia, MO 65211, USA.
authors: Anthony M
authors: AM
authors: Belenchia
authors: Aneesh K
authors: AK
authors: Tosh
authors: Laura S
authors: LS
authors: Hillman
authors: Catherine A
authors: CA
authors: Peterson
mesh_terms: D054392:Adipokines / Q000097:blood*; D052242:Adiponectin / Q000097:blood; D000293:Adolescent; D001786:Blood Glucose / Q000378:metabolism; D015992:Body Mass Index; D002648:Child; D002762:Cholecalciferol / Q000097:blood / Q000627:therapeutic use*; D019587:Dietary Supplements; D005260:Female; D006801:Humans; D018836:Inflammation Mediators / Q000097:blood; D007328:Insulin / Q000097:blood*; D007333:Insulin Resistance; D020738:Leptin / Q000097:blood; D008297:Male; D009765:Obesity / Q000097:blood / Q000150:complications*; D016896:Treatment Outcome; D014807:Vitamin D / Q000031:analogs & derivatives / Q000097:blood; D014808:Vitamin D Deficiency / Q000097:blood / Q000188:drug therapy* / Q000209:etiology; D014815:Vitamins / Q000097:blood / Q000627:therapeutic use
chemical_list: D054392:Adipokines; D052242:Adiponectin; D001786:Blood Glucose; D018836:Inflammation Mediators; D007328:Insulin; D020738:Leptin; D014815:Vitamins; D014807:Vitamin D; D002762:Cholecalciferol; C104450:25-hydroxyvitamin D