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dc.contributor.authorDutmanee Seriwatanachaien_US
dc.contributor.authorKanogwun Thongchoteen_US
dc.contributor.authorNarattaphol Charoenphandhuen_US
dc.contributor.authorJantarima Pandaranandakaen_US
dc.contributor.authorKukiat Tudporen_US
dc.contributor.authorJarinthorn Teerapornpuntakiten_US
dc.contributor.authorTuangporn Suthiphongchaien_US
dc.contributor.authorNateetip Krishnamraen_US
dc.contributor.otherMahidol Universityen_US
dc.contributor.otherFaculty of Medicine, Thammasat Universityen_US
dc.identifier.citationBone. Vol.42, No.3 (2008), 535-546en_US
dc.description.abstractHyperprolactinemia leads to high bone turnover as a result of enhanced bone formation and resorption. Although its osteopenic effect has long been explained as hyperprolactinemia-induced hypogonadism, identified prolactin (PRL) receptors in osteoblasts suggested a possible direct action of PRL on bone. In the present study, we found that hyperprolactinemia induced by anterior pituitary transplantation (AP), with or without ovariectomy (Ovx), had no detectable effect on bone mineral density and content measured by dual-energy X-ray absorptiometry (DXA). However, histomorphometric studies revealed increases in the osteoblast and osteoclast surfaces in the AP rats, but a decrease in the osteoblast surface in the AP + Ovx rats. The resorptive activity was predominant since bone volume and trabecular number were decreased, and the trabecular separation was increased in both groups. Estrogen supplement (E2) fully reversed the effect of estrogen depletion in the Ovx but not in the AP + Ovx rats. In contrast to the typical Ovx rats, bone formation and resorption became uncoupled in the AP + Ovx rats. Therefore, hyperprolactinemia was likely to have some estrogen-independent and/or direct actions on bone turnover. Osteoblast-expressed PRL receptor transcripts and proteins shown in the present study confirmed our hypothesis. Furthermore, we demonstrated that the osteoblast-like cells, MG-63, directly exposed to PRL exhibited lower expression of alkaline phosphatase and osteocalcin mRNA, and a decrease in alkaline phosphatase activity. The ratios of receptor activator of nuclear factor κB ligand (RANKL) and osteoprotegerin (OPG) proteins were increased, indicating an increase in the osteoclastic bone resorption. The present data thus demonstrated that hyperprolactinemia could act directly on bone to stimulate bone turnover, with more influence on bone resorption than formation. PRL enhanced bone resorption in part by increasing RANKL and decreasing OPG expressions by osteoblasts. © 2007 Elsevier Inc. All rights reserved.en_US
dc.rightsMahidol Universityen_US
dc.subjectBiochemistry, Genetics and Molecular Biologyen_US
dc.titleProlactin directly enhances bone turnover by raising osteoblast-expressed receptor activator of nuclear factor κB ligand/osteoprotegerin ratioen_US
Appears in Collections:Scopus 2006-2010

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