Poster Presentation Australian Diabetes Society and the Australian Diabetes Educators Association Annual Scientific Meeting 2017

Effects of vitamin D supplementation on inflammatory markers and nuclear factor kappa-B activity in vitamin D-deficient and overweight or obese adults: a randomized placebo-controlled trial. (#325)

Aya Mousa 1 , Negar Naderpoor 1 , Josphin Johnson 1 , Karly Sourris 2 , Maximilian de Courten 3 , Kirsty Wilson 4 , Robert Scragg 5 , Magdalena Plebanski 4 , Barbora de Courten 1
  1. Monash Centre for Health Research and Implementation, School of Public Health and Preventive Medicine, Monash University, Melbourne, VIC, Australia
  2. Baker Heart and Diabetes Institute, Melbourne, Victoria, Australia
  3. Centre for Chronic Diseases, Victoria University, Melbourne, VIC, Australia
  4. Department of Immunology and Pathology, Monash University, Melbourne, VIC, Australia
  5. School of Population Health, The University of Auckland, Auckland, New Zealand

BACKGROUND: In vitro studies suggest that vitamin D has anti-inflammatory properties which are thought to occur via inhibition of the nuclear factor kappa-B (NFκB) pathway. However, evidence from human trials is limited and no previous trials have investigated the effect of vitamin D supplementation on NFκB activity in vivo in humans. In a randomized placebo-controlled trial (RCT), we examined whether vitamin D supplementation would improve serum inflammatory markers and NFκB activity in peripheral blood mononuclear cells (PBMCs) in overweight or obese, otherwise healthy adults.

METHODS: Sixty-five overweight or obese (BMI≥25 kg/m2), vitamin D-deficient (25-hydroxyvitamin D (25(OH)D)≤50 nmol/l) adults were randomized to a bolus oral dose of 100,000IU followed by 4,000IU cholecalciferol daily or matching placebo for 16 weeks. Before and after intervention, we measured: serum 25(OH)D concentrations (chemiluminescent immunoassay); anthropometry: BMI, waist-to-hip ratio, %body fat (dual X-ray absorptiometry); serum pro- and anti-inflammatory markers: high-sensitivity C-reactive protein (hsCRP) (highly-sensitive immunoassay), tumour necrosis factor (TNF), monocyte chemoattractant protein-1 (MCP-1), interferon-gamma (IFN-γ) and interleukins (IL)-1β,-6 ,-8,-10,-18,-23,-33 (multiplex assay); NFκB activity in PBMCs (DNA-binding assay); dietary vitamin D intake, physical activity, and sun exposure (validated questionnaires).

RESULTS: Fifty-four participants completed the study (35M/19F; age=31.9±8.5 years; BMI=30.9±4.4 kg/m2). Serum 25(OH)D concentrations increased with vitamin D supplementation compared to placebo (57.0±21.3 versus 1.9±15.1 nmol/l;p<0.001). Change in hsCRP, TNF, MCP-1, IFN-γ, any of the interleukins, and NFκB activity did not differ between groups (all p>0.1). Results remained non-significant after adjustment for age, sex, and %body fat, and after further adjustment for sun exposure, physical activity, and dietary vitamin D intake (all p>0.1).

CONCLUSIONS: Although in vitro studies suggest that vitamin D can decrease inflammation via inhibiting NFκB activity, data from our RCT suggest that vitamin D supplementation has no effect on pro- or anti-inflammatory markers or in vivo NFκB activity in overweight or obese, otherwise healthy adults.