Interactions of insulin-like growth factor I with dexamethasone on trabecular bone density and mineral metabolism in rats
| Autor: | Roger Bouillon, Christoph Schmid, K Jürgensen, Ernst Rudolf Prof Dr Froesch, K Binz, E B Hunziker |
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| Rok vydání: | 1994 |
| Předmět: |
Blood Glucose
Male medicine.medical_specialty Bone disease Bone density Calcitriol Endocrinology Diabetes and Metabolism Osteocalcin Osteoporosis Bone and Bones Dexamethasone Bone remodeling Endocrinology Bone Density Osteoclast Internal medicine Weight Loss medicine Animals Humans Insulin Drug Interactions Insulin-Like Growth Factor I Cholecalciferol Minerals biology business.industry Vitamin D-Binding Protein Osteoblast General Medicine Alkaline Phosphatase medicine.disease Recombinant Proteins Rats medicine.anatomical_structure biology.protein business medicine.drug |
| Zdroj: | Scopus-Elsevier |
| ISSN: | 1479-683X 0804-4643 |
| DOI: | 10.1530/eje.0.1300387 |
| Popis: | Binz K, Schmid C, Bouillon R, Froesch ER, Jürgensen K, Hunziker EB. Interactions of insulin-like growth factor I with dexamethasone on trabecular bone density and mineral metabolism in rats. Eur J Endocrinol 1994;130:387–93. ISSN 0804–4643 Glucocorticoid treatment causes osteoporosis and growth retardation in humans. Insulin-like growth factor I (IGF-I) stimulates differentiation and replication of cultured osteoblast-like cells and induces longitudinal bone growth in IGF-I-deficient rats. We investigated the influence of subcutaneously infused IGF-I on bone and mineral metabolism of male rats treated with a high dose of dexamethasone. Dexamethasone was added to the drinking water in a concentration of 1 mg/l. After 30 days of dexamethasone treatment, recombinant human IGF-I (300 μg/day) or solvent was infused sc by osmotic minipumps for 21 days while dexamethasone was continued. Age-matched untreated male rats served as healthy controls. Dexamethasone-treated rats lost weight. Their IGF-I levels were decreased to 36% of healthy controls. Infusion of IGF-I resulted in an increase in IGF-I serum levels (582% compared to healthy controls) and allowed some weight gain. Osteocalcin and calcitriol levels were markedly decreased in dexamethasone-treated rats and were not influenced significantly by IGF-I infusion. In contrast, IGF-I treatment restored the free calcitriol concentration (molar ratio of calcitriol to vitamin D-binding protein) towards normal. Furthermore, infusion of IGF-I partially corrected the dexamethasone-induced hyperinsulinemia. Histomorphometric analysis revealed no difference in vertebral trabecular bone density (i.e. growth-independent bone remodeling) between the three groups. In contrast, mean trabecular bone density in tibial metaphyses was increased markedly by dexamethasone, presumably due to osteoclast inhibition. Insulin-like growth factor I infusion did not significantly influence these structural metaphyseal bone parameters. We conclude that IGF I-infusion in male rats treated with high doses of dexamethasone reduces insulin resistance and restores calcitriol production but not osteoblast function or responsiveness to calcitriol. K Binz, Division de Diabétologie, Hôpital Cantonal Universitaire, 1211 Geneva, Switzerland |
| Databáze: | OpenAIRE |
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