OSTEOPENIA ASSOCIATED WITH NON-INSULIN-DEPENDENT DIABETES-MELLITUS - WHAT ARE THE CAUSES

This study investigated whether alterations in bone mineral content (B MC) and/or in the phosphate-calcium metabolism exist in non-insulin-de pendent diabetes mellitus (NIDDM); whether they are linked to glycaemi c control and whether antidiabetic therapy - oral agents or insulin - influences BMC and mineral metabolism. A cross-section assessment comp ared BMC and mineral metabolism in 60 well-controlled and 50 poorly co ntrolled diabetic patients under oral hypoglycaemic therapy with 50 he althy controls. A longitudinal assessment improved the high glucose le vels of the poorly controlled diabetic group either by increasing oral treatment or by adding a bedtime NPH insulin. Glycaemic control, BMC and mineral metabolism were followed-up for 1 year. In NIDDM patients BMC is reduced. This reduction is more marked in poorly controlled dia betic patients. In well-controlled diabetes osteocalcin levels are low . In poorly controlled patients glycosuria, hypercalcuria and parathyr oid hyperactivity are present. In both groups vitamins 25(OH)-D, 1,25( PH)(2)-D and calcitonin levels are normal. Improving metabolic control increased BMC, normalized urinary calcium excretion and parathyroid a ctivity and reduced osteocalcin levels. The type of anti-diabetic ther apy does not have any significant effect upon BMC or upon phosphate-ca lcium metabolism. In conclusion, in NIDDM a hard-to-define osteoblast deficit appears to exist. In poorly controlled diabetes the loss of BM C is aggravated by the negative calcium balance caused by the renal ca lcium leak. This is due to glucosuric-induced osmotic diuresis and is maintained by parathyroid activation.