title: Cortisol mobilizes mineral stores from vertebral skeleton in the European eel: an ancestral origin for glucocorticoid-induced osteoporosis?
abstract: Endogenous excess cortisol and glucocorticoid (GC) therapy are a major cause of secondary osteoporosis in humans. Intense bone resorption can also be observed in other vertebrates such as migratory teleost fish at the time of reproductive migration and during fasting when large amounts of calcium and phosphate are required. Using a primitive teleost, the European eel, as a model, we investigated whether cortisol could play an ancestral role in the induction of vertebral skeleton demineralization. Different histological and histomorphometric methods were performed on vertebral samples of control and cortisol-treated eels. We demonstrated that cortisol induced a significant bone demineralization of eel vertebrae, as shown by significant decreases of the mineral ratio measured by incineration, and the degree of mineralization measured by quantitative microradiography of vertebral sections. Histology and image analysis of ultrathin microradiographs showed the induction by cortisol of different mechanisms of bone resorption, including periosteocytic osteolysis and osteoclastic resorption. Specificity of cortisol action was investigated by comparison with the effects of sex steroids. Whereas, testosterone had no effect, estradiol induced vertebral skeleton demineralization, an effect related to the stimulated synthesis of vitellogenin (Vg), an oviparous specific phospho-calcio-lipoprotein. By contrast, the cortisol demineralization effect was not related to any stimulation of Vg. This study demonstrates GC-induced bone demineralization in an adult non-mammalian vertebrate, which undergoes natural bone resorption during its life cycle. Our data suggest that the stimulatory action of cortisol on bone loss may represent an ancestral and conserved endocrine regulation in vertebrates.
authors.affiliation: Muséum National d'Histoire Naturelle, DMPA USM 0401, UMR 7208 CNRS BOREA Biologie des Organismes et Ecosystèmes Aquatiques, 7 rue Cuvier, CP 32, 75231 Paris Cedex 05, France.
authors.forename: Miskal
authors.initials: M
authors.lastname: Sbaihi
authors.forename: Karine
authors.initials: K
authors.lastname: Rousseau
authors.forename: Sylvie
authors.initials: S
authors.lastname: Baloche
authors.forename: François
authors.initials: F
authors.lastname: Meunier
authors.forename: Martine
authors.initials: M
authors.lastname: Fouchereau-Peron
authors.forename: Sylvie
authors.initials: S
authors.lastname: Dufour
mesh_terms: D000818:Animals; D005075:Biological Evolution; D001692:Biological Transport / Q000187:drug effects; D015519:Bone Density / Q000187:drug effects; D001862:Bone Resorption / Q000139:chemically induced; D002118:Calcium / Q000097:blood / Q000378:metabolism; D004524:Eels / Q000097:blood / Q000378:metabolism*; D005260:Female; D005938:Glucocorticoids / Q000009:adverse effects*; D012739:Gonadal Steroid Hormones / Q000494:pharmacology; D006854:Hydrocortisone / Q000494:pharmacology*; D008903:Minerals / Q000378:metabolism*; D010024:Osteoporosis / Q000139:chemically induced* / Q000378:metabolism; D010710:Phosphates / Q000097:blood / Q000378:metabolism; D013131:Spine / Q000187:drug effects* / Q000378:metabolism; D014819:Vitellogenins / Q000097:blood / Q000378:metabolism
chemical_list: D005938:Glucocorticoids; D012739:Gonadal Steroid Hormones; D008903:Minerals; D010710:Phosphates; D014819:Vitellogenins; D002118:Calcium; D006854:Hydrocortisone