Oral Presentation ANZOS-Breakthrough Discoveries Joint Annual Scientific Meeting 2018

Vitamin D supplementation improves adipokine concentrations in overweight or obese adults (#88)

Aya Mousa 1 , Negar Naderpoor 1 , Robert Scragg 2 , Barbora De Courten 1
  1. Monash Centre for Health Research and Implementation, School of Public Health and Preventive Medicine, School of Public Health and Preventive Medicine, Melbourne, VIC, Australia
  2. School of Population Health, The University of Auckland, Auckland, New Zealand

BACKGROUND: Adipokine dysregulation is a feature of obesity and related cardiometabolic disorders including type 2 diabetes. Vitamin D regulates adipokine production in vitro; however, clinical trials have been inconclusive.

OBJECTIVE: To examine the effects of vitamin D supplementation on serum adipokine concentrations in overweight or obese and vitamin D-deficient adults, using data from a randomized controlled trial (RCT).

DESIGN: Sixty-five individuals with a body mass index (BMI) ≥25 kg/m2 and 25-hydroxyvitamin D (25(OH)D) ≤50 nmol/L were randomized to an oral bolus dose of 100,000 IU followed by 4,000 IU daily of cholecalciferol or matching placebo for 16 weeks. Before and after the intervention, we measured BMI, waist-to-hip ratio (WHR), % body fat (dual energy X-ray absorptiometry), serum concentrations of 25(OH)D (chemiluminescent immunoassay) and total adiponectin, leptin, resistin, and adipsin (multiplex assay; flow cytometry). Sun exposure habits, physical activity, and diet were assessed using questionnaires.

RESULTS: Fifty-four participants completed the study (35M/19F; age=31.9±8.5 years; BMI=30.9±4.4 kg/m2 [mean±SD]). After 16 weeks, vitamin D supplementation increased serum 25(OH)D compared with placebo (57.0±21.3 versus 1.9±15.1 nmol/L, p<0.001). There were no differences between vitamin D and placebo groups for changes in adiponectin, leptin, resistin, or adipsin in unadjusted analyses (all p>0.05). After adjustment for baseline values, season, sun exposure, and dietary vitamin D intake, there was a greater increase in adiponectin (β [95%CI]= 13.7 [2.0, 25.5], p=0.02) and leptin (β [95%CI]= 22.3 [3.8, 40.9], p=0.02) concentrations in the vitamin D group compared with placebo. Results remained significant after additional adjustment for age, sex, and % body fat (both p<0.02).

CONCLUSIONS: Vitamin D may increase adiponectin and leptin concentrations in vitamin D-deficient and overweight or obese adults. Further studies are needed to clarify the molecular interactions between vitamin D and adipokines, and to establish the clinical implications of these interactions in the context of obesity.