For example, Aatsinki et al. (47) showed that vitamin D metabolizing enzymes are altered in experimentally induced diabetic states (both type 1 and type 2 diabetes), leading to the repression of vitamin D bioactivation and induction of deficiency, by the mechanisms that include the peroxisome proliferator-activated receptor-gamma coactivator 1-α and estrogen-related receptor α (PGC-1α-ERRα), and the glucocorticoid receptor pathways (47). Here, NR3C1 is linked to type 2 diabetes mellitus.