| Summary: | The role of vitamin D in obesity appears to be linked to vitamin D insufficient/deficient status. However, mechanistic understanding of the role of vitamin D in obesity is lacking. We have shown earlier that the vitamin D hormonal form, 1,25-dihydroxyvitamin D<sub>3</sub> (1,25(OH)<sub>2</sub>D<sub>3</sub>), induces cell death by apoptosis in mature adipocytes. This effect of the hormone is mediated by the cellular Ca<sup>2+</sup> signaling pathway: a sustained increase of intracellular (cytosolic) Ca<sup>2+</sup> concentration followed by activation of Ca<sup>2+</sup>-dependent initiators and effectors of apoptosis. In recent animal studies, we demonstrated that low vitamin D status is observed in diet-induced obesity (DIO). High intake of vitamin D<sub>3</sub> in DIO decreased the weight of white adipose tissue and improved biomarkers related to adiposity and Ca<sup>2+</sup> regulation. The anti-obesity effect of vitamin D (1,25(OH)<sub>2</sub>D<sub>3</sub>) in DIO was determined by the induction of Ca<sup>2+</sup>-mediated apoptosis in mature adipocytes executed by Ca<sup>2+</sup>-dependent apoptotic proteases (calpains and caspases). Thus, a high intake of vitamin D in obesity increases vitamin D nutritional status and normalizes vitamin D hormonal status that is accompanied by the reduction of adiposity. Overall, our findings imply that vitamin D may contribute to the prevention of obesity and obesity-related diseases and that the mechanism of the anti-obesity effect of 1,25(OH)<sub>2</sub>D<sub>3</sub> includes induction of Ca<sup>2+</sup>-mediated apoptosis in adipocytes.
|
|---|
