BONE-MINERAL LOSS IN INSULIN-TREATED DIABETES-MELLITUS - STUDIES ON PATHOGENESIS

To elucidate pathogenetic factors of bone mineral loss in diabetes mellitus, bone mineral content (BMC), glucose and calcium homeostasis were evaluated in a cross-sectional study of 215 insulin-treated diabetics. BMC declined 10% during the first 5 years of diabetes. This coincided with cessation of insulin secretion, deterioration of metabolic control and raiding urinary excretion rates of calcium and phosphorus. BMC was inversely correlated to fasting blood glucose (P<0.02), to glycosuria (P<0.02) and to insulin requirement (P<0.002), and positively to the glucagon-stimulated serum C-peptide levels (P<0.005). Urinary excretion rates of calcium and phosphorus correlated positively with the degree of hyperglycaemia (P<0.001) and glycosuria (P<0.001). The skeletal calcium loss corresponded to the excess of urinary calcium excretion during the phase of BMC reduction. There was no evidence of secondary hyperparathyroidism. The relationship between bone loss and disturbed glucose homeostasis indicates that diabetic bone loss is secondary to the metabolic abnormalities, possibly acting directly on bone.