Reduced bone mass occurring with increased frequency in diabetes mellitus has been attributed to poor blood glucose control but the pathogenetic mechanisms remain unknown. To evaluate the role of calcium metabolism, 59 patients with diabetes and normal renal function (22 Type 1, 37 Type 2) were studied. In all patients plasma calcium (Ca), serum phosphate (PO4), serum parathyroid hormone (PTH), and 24-h urinary calcium (uCa) were determined under both poor and improved control (for at least 7 days) as ascertained by four blood glucose determinations daily. Improvement of blood glucose control (p = 0.001) was associated with reduction of uCa both in Type 1 (6.9 +/- 1 vs 4.9 +/- 0.9 mmol day-1, mean +/- SEM, p = 0.02) and in Type 2 patients (4.2 +/- 0.4 vs 3.2 +/- 0.4 mmol day-1, mean +/- SEM, p = 0.002). Considerably more Type 1 patients (10 out of 22) had PTH values below the detection limit (1.5 pmol l-1) during poor than during improved control (2 out of 22). Comparison between the two types of diabetes showed that in Type 1 under poor control, Ca and PTH were lower (p = 0.03), while uCa was higher (p = 0.003), and after improved control, only uCa continued to be higher (p = 0.035). These findings suggest that increased uCa excretion in association with 'functional hypoparathyroidism' (especially in Type 1 diabetes) is observed during poor blood glucose control, and may be one of the factors leading to reduced bone mass in diabetes mellitus.