Background & Aims: Low serum 25-hydroxyvitamin D (25OHD) is common in obesepeople. Obesity is associated with a state of low-grade inflammation (meta-inflammation). There is an increasing evidence indicating that vitamin D has anti-adipogenic activity and immunoregulatory effect. This study aimed to assess the effect of vitamin D supplementation on meta-inflammation and fat mass in obese subjects with vitamin D deficiency.
Materials and methods:In this double-blind placebo-controlled randomized clinical trial, 44 obese subjects with vitamin D deficiency (25OHD < 50 nmol/L) were assigned into vitamin D (a weight reduction diet + bolus weekly dose of 50 000 IU vitamin D) or placebo group (weight reduction diet + edible paraffin weekly) for 12 weeks.Weight, fat mass and serum levels of 25OHD, calcium, parathyroid hormone (PTH), monocyte chemoattractant protein-1 (MCP-1), interleukin-1β (IL-1β) and Toll-like receptor 4 (TLR4) were assessed before and after the intervention.Results: Vitamin D supplementation resulted in significant increase of serum 25OHD level (P < 0.001), and significant decrease in PTH (P < 0.001), MCP-1 (P < 0.05), IL-1β (P < 0.05) and TLR-4 (P < 0.05); compared to the baseline values in vitamin D group.Weight, BMI and fat mass decreased in both groups (P < 0.05). Between the groups, there were significant decrease in weight, fat mass, serum MCP-1 and PTH concentrations and significant increase in serum 25OHD concentrations after intervention with vitamin D supplementation compared to placebo (P < 0.05).Conclusions: Improvement in vitamin D status in obese subjects with vitamin D deficiency in combination with weight loss diet resulted in weight, fat mass and MCP-1 decrease. Weight loss and vitamin D supplementation may act synergistically to reduce levels of meta-inflammation.
K E Y W O R D Sfat mass, meta-inflammation, obesity, vitamin D supplementation, weight loss | 95 LOTFI-DIZAJI eT AL.
As there is limited and inconsistent evidence in potential role of vitamin D on insulin resistance and matrix metalloproteinases, this study aimed to examine the effect of vitamin D supplementation on glucose homeostasis, insulin resistance and matrix metalloproteinases in obese subjects with vitamin D deficiency. A total of 44 participants with serum 25(OH)D level ≤ 50 nmol/L and body mass index (BMI) 30-40 kg/m2 were randomly allocated into receiving weight reduction diet with either 50000 IU vitamin D3 pearl (n = 22) or placebo (n = 22) once weekly for 12 weeks. Primary outcomes were changes in fasting serum glucose (FSG), homeostasis model assessment insulin resistance (HOMA-IR), quantitative insulin sensitivity check index (QUICKI) and matrix metalloproteinases (MMPs). Secondary outcomes were changes in weight, body mass index (BMI), 25(OH) D, calcium, phosphorous and Parathyroid hormone (PTH). Sun exposure and dietary intakes were also assessed. Serum levels of 25(OH) D3 increased significantly with a simultaneous decrease in serum concentration of PTH in vitamin D group. Weight, BMI, FSG and MMP-9 decreased significantly in both groups; while there were found significant differences in changes in weight, serum 25(OH) D3, PTH and MMP-9 levels between the groups. Within and between groups analysis revealed no significant differences in serum calcium, phosphorous, serum insulin, HOMA-IR, QUICKI and MMP-2 after intervention. Our results indicated that improvement in vitamin D status resulted in greater reductions in weight and MMP-9 during weight loss. These preliminary results are sufficient to warrant a bigger study group.
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