Calcium intake regulates 1,25-dihydroxy-vitamin D formation in the diabetic rat.

Duodenal calcium absorption and serum 1,25-dihydroxyvitamin D [1,25-(OH)2D] concentrations are decreased and body growth is arrested in the streptozotocin-diabetic rat taking commercial chow with high (1.2-2%) calcium content. Treatment with insulin restores 1,25-(OH)2D3, calcium absorption, and body growth to normal. We hypothesized that the depressed 1,25-(OH)2D3 in diabetics is due in part to the minimal requirement for vitamin-D-mediated intestinal calcium transport under conditions of arrested growth and high calcium intake. We tested this hypothesis by comparing the response of serum 1,25-(OH)2D3 concentration to low (0.02%) and normal (0.5%) calcium diets in control and streptozotocin-diabetic rats. To evaluate response to short-term insulin treatment, serum 1,25-(OH)2D3 was measured after 12 or 36 h of treatment. Serum 1,25-(OH)2D3 concentrations in the 0.5% calcium diet groups were 175, 25, and 120 pg/ml for control, diabetic, and insulin-treated 36-h groups, respectively. Low calcium diets increased concentration to 625, 100, and 370 pg/ml for controls, diabetics, and insulin-treated 36-h groups, respectively. In conclusion, the diabetic retains the ability to respond to calcium deficiency, even in the insulin-deficient state. Low calcium intake, in addition to enhancing 1,25-(OH)2D3 formation in diabetics, also modulates the response to insulin treatment. These studies demonstrate that the regulatory factor(s) suppressing serum, 1,25-(OH)2D3 in diabetes is not simply insulin deficiency per se. Implications of these findings for diabetes are discussed.