1, (1,25(OH) 2 D 3 ) concentrations have been found to be decreased in diabetic humans and rats. To investigate further the regulation of plasma Ca in diabetes, first we measured Ca 2+ , P, Mg, parathyroid hormone 1-34 (PTH), and total and free 1,25(OH) 2 D 3 in male spontaneously diabetic rats 7 and 28 days after the onset of glycosuria. Secondly, we studied changes in the levels of PTH and 1,25(OH) 2 D 3 in response to hypocalcaemia induced by an i.v. infusion of EGTA (2·5%, wt/vol.) for 24 h, and changes in the levels of 1,25(OH) 2 D 3 in response to an i.v. infusion of rat PTH (10 ”g over 24 h) without or with concomitant EGTA infusion (producing hypercalcaemia or normo/ hypocalcaemia respectively), in diabetic and control rats. Ca 2+ , P, Mg and PTH concentrations remained within the control ranges after 7 and 28 days of glycosuria; 1,25(OH) 2 D 3 concentrations were decreased after 7, but not after 28, days of glycosuria. PTH concentrations showed a similar rise during EGTA-induced hypocalcaemia in control and diabetic rats compared with salineinfused rats, whereas 1,25(OH) 2 D 3 concentrations were unchanged in both groups. Total and free 1,25(OH) 2 D 3 levels were comparably (about 3-fold) increased during PTH, but not during combined PTH and EGTA infusion in control and diabetic rats. Total 1,25(OH) 2 D 3 concentrations were lower in the diabetic groups infused with saline or PTH than in their respective controls, and there was a similar trend in the PTH+EGTA-infused group; free 1,25(OH) 2 D 3 levels, however, were normal or increased in the diabetic groups, confirming our previous data.The novel finding of this study is that, despite severe insulin deficiency and altered 1,25(OH) 2 D 3 levels, the in vivo response of PTH levels to hypocalcaemia and the in vivo response of 1,25(OH) 2 D 3 levels to PTH in diabetic rats are comparable with those found in nondiabetic rats.