Prospective bone mineral density evaluation in patients with insulin-dependent diabetes mellitus.

The bone mineral density (BMD) in patients with insulin-dependent diabetes mellitus (IDDM) was evaluated prospectively to assess the course of osteopenia in IDDM. We measured BMD in the lumbar spine, femoral region, and total body calcium in 23 patients aged 21-53 years with IDDM for 2.3 to 20 years using a dual energy X-ray absorptiometry. A second BMD measurement was done after 26.5+/-4.1 months in all patients. The blood glucose control, insulin dosage, and disease duration were also assessed. Eleven patients had osteopenia (1 Z-score below the mean values of normal gender- and age-matched individuals). These patients had a longer IDDM duration (8.6+/-5.1 years in osteopenics versus 4.6+/-3.75 years in non-osteopenics; p=0.03). The blood glucose control and insulin dosage were not significantly different throughout the study. The mean spinal BMD was higher in the second evaluation in both osteopenics (0.91+/-0.12 g/cm2 and 0.96+/-0.09 g/cm2, p=0.035) and non-osteopenics (1.24+/-0.15 g/cm2 and 1.29+/-0.16 g/cm2; p=0.02). In the end of the study, however, the osteopenic group persisted with lower subnormal BMD values than the non-osteopenic group (p < 0.001). The small BMD increment observed in the spine did not correlate with changes in the metabolic control or with IDDM duration, but occurred mainly in patients younger than 30 years old. There was no significant change in the femoral BMD or total body calcium. None of the patients developed or significantly worsened the osteopenia. We conclude that diabetic osteopenia, despite being a complication of high prevalence in IDDM, seems to be non-progressive in the majority of patients. In some patients, the spinal BMD increased during observation and may have been due to achievement of peak bone mass.

True insulin and intact proinsulin levels in acromegalic patients.

To determine whether proinsulin (PI) contributes significantly to the immunoreactive insulin (IRI) concentrations in acromegalics, we measure PI, "true insulin" and IRI in a group of acromegalics compared with a control group. Serum PI was determined by the immunofluorimetric assay (IFMA). Insulin was also determined by an IFMA that measures true insulin and by a radioimmunoassay (RIA). We performed an oral glucose tolerance test (OGTT) in a total group of 46 subjects: 10 controls with normal OGTT and body mass index < 25 kg/m2 (control group I), 10 controls with normal OGTT and body mass index > 25 kg/m2 (control group II), 15 patients with active acromegaly and normal OGTT and 11 patients with active acromegaly and IGT. Plasma glucose, serum GH, insulin and proinsulin were measured in all OGTT samples. Basal levels of insulin-like growth factor I (IGF-I) were measured in acromegalics. Mean body mass index in acromegalics with normal and impaired glucose tolerance were significantly higher compared with control group I and similar when compared with control group II. Proinsulin increased during OGTT in acromegalics with impaired glucose tolerance compared to control group I, and only fasting proinsulin compared to control group II. In normal OGTT acromegalics, only fasting proinsulin was increased. The RIA insulin during OGTT was significantly higher for both acromegalic groups compared to control group I and only at fasting when compared with control group II. This difference was not evident when insulin was measured by IFMA. These results suggest that in acromegalics, hyperinsulinism measured by RIA was at least in part due to hyperproinsulinism.