期刊
JOURNAL OF TRANSLATIONAL MEDICINE
卷 11, 期 -, 页码 -出版社
BIOMED CENTRAL LTD
DOI: 10.1186/1479-5876-11-271
关键词
IGF-I; GH; Bone metabolism; Gene expression; Osteocalcin; Osteoprotegerin; Parathormone; RANKL; IGFBP-4; IGFBP-5
资金
- Spanish I + D Program [SAF 2009-08319]
Background: Bone is one of the major target tissues for Insulin-like Growth Factor I (IGF-I). Low doses of IGF-I were able to improve liver-associated osteopenia. In the present work, a model of partial IGF-I deficiency was used in order to provide insight into the mechanisms of the beneficial actions of IGF-I replacement therapy in bone. Methods: Several proteins involved in osteoblastic/osteocyte and osteoclastic differentiation and activity were studied in the three experimental groups: control (CO) group (wild type mice, Igf(+/+), n = 10), heterozygous Igf(+/-) group with partial IGF-I deficiency (Hz, n = 10), and heterozygous Igf +/-mice treated with IGF-I for 10 days (Hz + IGF-I, n = 10). Results: Data in this paper confirm that the simple partial IGF-I deficiency is responsible for osteopenia, determined by densitometry and histopathology. These findings are associated with a reduced gene expression of osteoprotegerin, sclerostin, calcitonin receptor (CTR), insulin-like growth factor binding protein 5 and RUNX2. IGF-I replacement therapy normalized CTR gene expression and reduced markers of osteoclastic activity. Conclusions: Low doses of IGF-I constituted a real replacement therapy that normalized IGF-I serum levels improving the expression of most of these proteins closely involved in bone-forming, and reducing bone resorption by mechanisms related to osteoprotegerin, RANKL and PTH receptor.
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