title: [Bone metabolism by sex hormones and gonadotropins].
abstract: Pathophysiology of postmenopausal osteoporosis has been considered due to deficiency of estrogen. However, it has been reported that the rate of bone mass loss during perimenopause is greater than that in postmenopause, probably due to increased FSH. From the recent knowledge of basic research on FSH, FSH can directly stimulate osteoclast formation and accelerate bone resorption. In contrast, FSH transgenic mice exhibit increased bone mass dependent on ovarian function. In this review, the controversies on the function of FSH in bone mass regulation will be discussed.
authors.affiliation: Division of Integrative Pathophysiology, Proteo-Science Center,Graduate School of Medicine, Ehime University, Japan.
authors.forename: Yuuki
authors.initials: Y
authors.lastname: Imai
mesh_terms: D000818:Animals; D015519:Bone Density; D001862:Bone Resorption; D001842:Bone and Bones / Q000378:metabolism*; D004967:Estrogens / Q000172:deficiency / Q000502:physiology; D005640:Follicle Stimulating Hormone / Q000502:physiology*; D006062:Gonadotropins / Q000378:metabolism*; D006801:Humans; D010010:Osteoclasts; D015663:Osteoporosis, Postmenopausal / Q000378:metabolism; D053245:RANK Ligand; D011962:Receptors, FSH / Q000502:physiology
chemical_list: D004967:Estrogens; D006062:Gonadotropins; D053245:RANK Ligand; D011962:Receptors, FSH; D005640:Follicle Stimulating Hormone