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Calcitonin secretion in children with insulin-dependent diabetes mellitus
G Saggese1, S Bertelloni, G I Baroncelli
1Department of Paediatrics, University of Pisa, Italy.
Insights
Calcitonin (CT) deficiency does not cause bone loss in insulin-dependent diabetes mellitus (IDDM). Children with IDDM showed reduced CT reserve, suggesting increased bone reabsorption stimulates CT secretion.
Area of Science:
- Endocrinology
- Metabolic Bone Disease
- Pediatric Endocrinology
Background:
- Insulin-dependent diabetes mellitus (IDDM) is associated with bone mineral loss.
- The role of calcitonin (CT) deficiency in diabetic osteopenia is unclear.
Purpose of the Study:
- To investigate if calcitonin deficiency contributes to bone mineral loss in children with IDDM.
- To assess basal and calcium-stimulated calcitonin levels in diabetic children with osteopenia.
Main Methods:
- Studied 15 children with IDDM and osteopenia and 10 healthy controls.
- Measured total serum CT (tCT) and extractable CT (exCT) levels.
- Administered a calcium stimulation test to assess CT reserve.
Main Results:
- Diabetic children had slightly higher basal tCT and exCT levels than controls.
- Calcium stimulation increased CT levels in both groups, but diabetic children showed a reduced CT reserve (lower peak/basal ratio).
- Diabetic children exhibited a more rapid decrease in CT levels post-stimulation.
Conclusions:
- Calcitonin deficiency is not a cause of osteopenia in IDDM.
- Slightly elevated basal CT suggests increased bone reabsorption in IDDM, stimulating CT secretion.
- Chronic stimulation may lead to the observed reduction in CT reserve.
Abstract:
To test the hypothesis that calcitonin (CT) deficiency may contribute to bone mineral loss in insulin-dependent diabetes mellitus (IDDM), we studied basal and calcium stimulated (2 mg/kg body wt. in 5 min) CT levels in 15 children with IDDM and osteopenia. Ten age-sex matched healthy children were studied as controls. Since extractable CT (exCT) allows more sensitive and specific measurement of CT monomer, we measured both total serum CT (tCT) and exCT. Diabetic children had slightly but significantly (P less than 0.05) higher basal levels of both tCT (24.5 +/- 7.1 ng/l) and exCT (5.6 +/- 1.6 ng/l) than controls (tCT: 18.7 +/- 5.4 ng/l; exCT: 4.3 +/- 1.2 ng/l). Calcium stimulation test pointed out significant increase (P less than 0.001) of tCT and exCT in both groups with peak values not significantly different in IDDM in respect to controls. However, diabetic children showed a reduced CT reserve evidenced by a lower peak/basal ratio (diabetics: tCT 1.68, exCT 1.84; controls: tCT 2.49, exCT 2.88) and by a more rapid decrease in CT levels. We conclude that CT deficiency is not a causative factor of diabetic osteopenia. The slightly higher basal CT values suggest that an increased bone reabsorption may be operative in IDDM and it stimulates CT secretion. This chronic "C" cell stimulation may induce the reduction in CT reserve observed employing the calcium infusion test.