The hormone 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] induces cellular Ca2+ signals which regulate insulin secretion, while low vitamin D status may be a risk factor for type 2 diabetes (T2D). In pancreatic β-cells in vitro, 1,25(OH)2D3 induces, via multiple Ca2+ signaling pathways, synchronous Ca2+ oscillations, which quantitatively, temporally, and spatially pattern pulsatile insulin secretion from these cells. In animal studies employing a high fat diet-induced obesity model of pre-T2D, an increased intake of vitamin D delayed development of T2D and adiposity and was associated with the improved blood markers of diabetes and the vitamin D nutritional and hormonal status [plasma concentrations of glucose, insulin, adiponectin, 25-hydroxyvitamin D, and 1,25(OH)2D3]. Observational studies demonstrated associations between vitamin D status, insulin secretion and resistance to T2D, however, randomized controlled trials did not provide conclusive insights into the potential role of vitamin D in prevention of T2D. The 1,25(OH)2D3-dependent cellular Ca2+ signaling can be important for maintaining the normal level of insulin secretion from pancreatic β-cells, and an increased intake of vitamin D may contribute to the prevention of T2D and metabolic disorders associated with this disease.