Calcitriol improves streptozotocin-induced diabetes and recovers bone mineral density in diabetic rats

Vitamin D analogs exert a preventative effect on experimental diabetes, but whether or not they are able to halt progress of established diabetes is not yet known. Moreover, it is widely accepted that diabetes may induce osteoporosis, but the efficacy of vitamin D on diabetic osteoporosis is not cle...

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Bibliographic Details
Published in:Calcified tissue international 2004-12, Vol.75 (6), p.526-532
Main Authors: Del Pino-Montes, J, Benito, G E, Fernández-Salazar, M P, Coveñas, R, Calvo, J J, Bouillon, R, Quesada, J M
Format: Article
Language:English
Subjects:
Absorptiometry, Photon
Animals
Bone Density - drug effects
Bone Diseases, Metabolic - chemically induced
Bone Resorption - chemically induced
Calcitriol - metabolism
Calcium - blood
Diabetes Mellitus, Experimental - blood
Diabetes Mellitus, Experimental - metabolism
Diabetes Mellitus, Experimental - pathology
Female
Lumbar Vertebrae
Pancreas - pathology
Rats
Rats, Wistar
Tibia
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Summary:Vitamin D analogs exert a preventative effect on experimental diabetes, but whether or not they are able to halt progress of established diabetes is not yet known. Moreover, it is widely accepted that diabetes may induce osteoporosis, but the efficacy of vitamin D on diabetic osteoporosis is not clear. In order to help clarify these issues, we have tested the efficacy of calcitriol streptozotocin-induced diabetes. Streptozotocin (60 mg/Kg body weight) was injected in 3-month-old Wistar rats, randomly distributed into two groups: vehicle (olive oil) treated diabetic rats (D) and diabetic rats treated with 1.25-(OH)2D3 250 mg, three times a week (DT). Control animals (C) were treated with vehicle alone. The experiment lasted 8 weeks. The histology of the pancreata was evaluated. Blood glucose and calcium and phosphate in serum and urine were measured. Finally, bone mineral density (BMD) of tibia and lumbar vertebrae were evaluated. After 8 weeks, diabetes persisted in 85% of the diabetic rats (D group), but in only 45% of vitamin D-treated group (DT). At the end of the experiment, DT animals were separated into two groups, those still remaining diabetic (DT-NR) and reversed animals (DT-R). Moreover, bone loss was observed in diabetic animals (D), whereas BMD of DT-R rats showed similar values to those of controls (C). Our results suggest that 1.25(OH)2D3 improves diabetes and, as such, may recover BMD in streptozotocin-induced diabetic rats.
ISSN:0171-967X
1432-0827
DOI:10.1007/s00223-004-0118-9