Editorial

Can the sunshine vitamin melt the fat?

Vitamin D deficiency (VDD) is prevalent worldwide. This chapter discusses the association between VDD and metabolic syndrome (MetS). The widespread distribution of vitamin D receptors (VDRs) in various tissues (including cardiomyocytes, vascular endothelial and smooth muscle cells, dendritic cells, T-cells, and macrophages) provides a definitive basis to look into this association. The delineation of such pathways may provide insights into newer means to tackling the rising global burden of non-communicable diseases. This chapter serves to update the reader on current knowledge on the association between Vitamin D and individual components of the MetS (central obesity, hypertension, diabetes, dyslipidemia) including the newer proposed components like nonalcoholic steatohepatitis (NASH) and polycystic ovarian syndrome (PCOS). Various intervention studies of vitamin D supplementation in adults and children are also described along with prospects of a possible therapeutic role giving a peek into the future directions for research in this area.

Vitamin D insufficiency is common in subjects with type 2 diabetes. Observational studies suggest that vitamin D plays a role in the pathogenesis of type 2 diabetes. However, results of intervention studies have been inconsistent. We investigated the effects of improving vitamin D status on insulin sensitivity, insulin secretion, and inflammatory markers in patients with type 2 diabetes.

A double blind, randomized, placebo controlled trial was conducted. Sixteen patients with type 2 diabetes and hypovitaminosis D were recruited. Eight patients received colecalciferol and (280 μg daily for 2 weeks, 140 μg daily for 10 weeks) and 8 patients received identical placebo tablets for 12 weeks. Before and after intervention, patients underwent IVGTT, hyperinsulinemic euglycemic clamp, assessment of baseline high-frequency insulin pulsatility, glucose-entrained insulin pulsatility, DXA scans, 24-hour-ambulatory blood pressure monitorings, and fasting blood samples.

Serum-25(OH) vitamin D and serum-1,25(OH)₂ vitamin D increased significantly after 12 weeks in the intervention group (p = 0.01, p = 0.004). Serum-25(OH) vitamin D was also significantly higher in the vitamin D group compared to the placebo group (p = 0.02) after intervention. Although no significant changes in insulin sensitivity, inflammation, blood pressure, lipid profile, or HbA1c were found, we observed borderline (p between 0.05 and 0.10) improvements of insulin secretion, in terms of c-peptide levels, first phase incremental AUC insulin and insulin secretory burst mass.

Improvement in vitamin D status does not improve insulin resistance, blood pressure, inflammation or HbA1c, but might increase insulin secretion in patients with established type 2 diabetes.