Bone mineral metabolism in human type 1 (insulin dependent) diabetes mellitus.

Decreased bone mineral content has been observed in several studies of type 1 (insulin-dependent) diabetics in comparison with age and sex matched control subjects. In type 2 diabetics contradictory results have been obtained, probably related to varying degrees of body overweight in the patients investigated. The decrease in bone mineral content in type 1 diabetics was most pronounced in patients with childhood or adolescent onset of the disease, with ceased beta-cell function, with high insulin dosage, and poor glucose regulation. In a subgroup of patients having all these "risk factors" bone mineral content was decreased some 20%, as compared with patients without any "risk factors", and/or with sex and age matched controls. Bone mineral homeostasis was characterized by increased urinary excretions of bone minerals (calcium, phosphate and magnesium) related to the degree of hyperglycaemia and insulin dosage, by decreased serum concentrations of ionized calcium and magnesium, by increased to normal serum concentrations of phosphate, by a low-normal serum concentration of parathyroid hormone, and by a low-normal serum concentration of 1,25-dihydroxyvitamin D. This indicates a state of functional hypoparathyroidism in type 1 diabetics. Several mechanisms may thus contribute to diabetic osteopenia: Proneness to metabolic acidosis, hypocalcaemia, insulin deficiency and perhaps also hypomagnesaemia and hypoparathyroidism.