{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2024,3,14]],"date-time":"2024-03-14T00:18:42Z","timestamp":1710375522215},"reference-count":45,"publisher":"Oxford University Press (OUP)","issue":"3","license":[{"start":{"date-parts":[[1996,3,1]],"date-time":"1996-03-01T00:00:00Z","timestamp":825638400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/journals\/pages\/open_access\/funder_policies\/chorus\/standard_publication_model"}],"funder":[{"name":"Endocrine Laboratory"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[1996,3,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>To evaluate the osteoblastic function in patients with multiple pituitary hormone deficiencies (M-PHD) and with isolated growth hormone deficiency (I-GHD), bone cells were cultured and the effects of 10\u22128 M 1,25-dihydroxyvitamin D3 (1,25[OH]2D3) on parameters of cell proliferation, osteoblastic differentiation, and local paracrine regulation were measured. Three days of 1,25(OH)2D3 treatment increased alkaline phosphatase activity and osteocalcin release but inhibited [3H]thymidine incorporation in all cell cultures from patients as well as from controls. In addition, 1,25(OH)2D3 increased the release of both total and active transforming growth factor-\u03b2 (TGF-\u03b2) in bone cells from controls by, respectively, 4.9- and 3.2-fold and in bone cells from I-GHD by 5.1- and 1.5-fold, respectively. However, in bone cells from M-PHD, the stimulation of total TGF-\u03b2 release was significantly lower (1.3-fold) than in control and I-GHD cells, and active TGF-\u03b2 release was not stimulated at all. One year of supplementation with human growth hormone did not improve this deficient TGF-\u03b2 release in bone cells from M-PHD. We conclude that cultured bone cells from I-GHD and M-PHD show a normal response to 1,25(OH)2D3 regarding cell proliferation and osteoblastic differentiation, which implicates a normal l,25(OH)2D3-receptor function. In cells from controls and I-GHD, 1,25(OH)2D3 enhanced both total and active TGF-\u03b2 release. However, bone cells from M-PHD showed a deficient TGF-\u03b2 response to 1,25(OH)2D3. These results suggest that the regulation of TGF-\u03b2 production is a major paracrine factor involved in hypopituitarism.<\/jats:p>","DOI":"10.1002\/jbmr.5650110310","type":"journal-article","created":{"date-parts":[[2010,2,3]],"date-time":"2010-02-03T15:31:40Z","timestamp":1265211100000},"page":"367-376","source":"Crossref","is-referenced-by-count":15,"title":["1,25-Dihydroxyvitamin D3\u2014mediated transforming growth factor-\u03b2 release is impaired in cultured osteoblasts from patients with multiple pituitary hormone deficiencies"],"prefix":"10.1093","volume":"11","author":[{"given":"Jozien G. 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