@article{PAR00009928,
  title = {{C}ortisol mobilizes mineral stores from vertebral skeleton in the {E}uropean eel: an ancestral origin for glucocorticoid-induced osteoporosis?},
  author = {{S}baihi, {M}. and {R}ousseau, {K}. and {B}aloche, {S}. and {M}eunier, {F}. and {F}ouchereau-{P}eron, {M}. and {D}ufour, {S}ylvie},
  editor = {},
  language = {{ENG}},
  abstract = {{E}ndogenous excess cortisol and glucocorticoid ({GC}) therapy are a major cause of secondary osteoporosis in humans. {I}ntense 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. {U}sing a primitive teleost, the {E}uropean eel, as a model, we investigated whether cortisol could play an ancestral role in the induction of vertebral skeleton demineralization. {D}ifferent histological and histomorphometric methods were performed on vertebral samples of control and cortisol-treated eels. {W}e 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. {H}istology and image analysis of ultrathin microradiographs showed the induction by cortisol of different mechanisms of bone resorption, including periosteocytic osteolysis and osteoclastic resorption. {S}pecificity of cortisol action was investigated by comparison with the effects of sex steroids. {W}hereas, testosterone had no effect, estradiol induced vertebral skeleton demineralization, an effect related to the stimulated synthesis of vitellogenin ({V}g), an oviparous specific phospho-calciolipoprotein. {B}y contrast, the cortisol demineralization effect was not related to any stimulation of {V}g. {T}his study demonstrates {GC}-induced bone demineralization in an adult non-mammalian vertebrate, which undergoes natural bone resorption during its life cycle. {O}ur data suggest that the stimulatory action of cortisol on bone loss play represent an ancestral and conserved endocrine regulation in vertebrates. {J}ournal of {E}ndocrinology (2009) 201, 241-252},
  keywords = {},
  booktitle = {},
  journal = {{J}ournal of {E}ndocrinology},
  volume = {201},
  numero = {2},
  pages = {241--252},
  ISSN = {0022-0795},
  year = {2009},
  DOI = {10.1677/joe-08-0492},
  URL = {https://www.documentation.ird.fr/hor/{PAR}00009928},
}