Based on experience from experimental and human studies, vitamin D can be considered an important factor lowering the risk of diabetes mellitus type 1 and 2. The mechanism consists in the direct influence of vitamin D via nuclear receptors on genes coding proteins associated with normal function of B cells of Langerhans islands and genes coding proteins ensuring normal function of the immune system. There is also an indirect influence via regulation of homeostasis of calcium. Clinical observation and cross-sectional studies show an inverse relationship between vitamin D deficiency and appearance of diabetes mellitus type 2. A major deficit of vitamin D in diabetes mellitus type 2 appears to be an independent factor able to predict an increased risk of future cardiovascular mortality. Deficiency in early periods of life was shown to precede autoimmune diabetes mellitus type 1 in an experiment as well as in humans. Prevention of vitamin D deficiency in early as well as later periods of life is a basic pre-requisites of successful preventive measures against diabetes mellitus type 1. Explicit evidence for the significance of the correction of vitamin D deficiency for improvement of metabolic control in diabetics is still missing mainly due to a low number of intervention, placebo-controlled and randomized trials. On the other side, intervention studies often showed positive influence on the conditions accompanying diabetes, such as systolic hypertension or endothelial dysfunction. Unlike in diabetics, the intervention trials showed positive results in non-diabetics with high risk of type 2 diabetes and impaired fasting glycaemia or insulin resistance. One can conclude that existing knowledge already indicate that maintaining the level of 25-hydroxyvitamin D > 30 ng/ml during the year without seasonal variations will be have multiple real as well as potential health benefits. A great promise for clinical practice are the structural analogs of vitamin D tested experimentally, which maintain the influence on the immune system, effect of insulin and B cells function, but have suppressed influence on bone and calcium metabolism.