Show simple item record Szabó, András Merke J Thomasset M Ritz E 2018-10-12T08:50:42Z 2018-10-12T08:50:42Z 1991
dc.identifier 0026091082
dc.identifier.citation pagination=521-526; journalVolume=21; journalIssueNumber=5; journalTitle=EUROPEAN JOURNAL OF CLINICAL INVESTIGATION;
dc.description.abstract In parathyroids of uraemic patients or animals, decreased specific binding of 1,25(OH)2D3 has been observed and implicated in the genesis of secondary hyperparathyroidism of renal failure. We re-examined binding of 1,25(OH)2D3 using chromatin preparations for receptor characterization which differed from previous studies (a) by inclusion of protease inhibitors (PMSF, aprotinin) and molybdate in the extraction buffer and (b) by omitting the K-extraction step. With this method, the Nmax in the intestinal mucosa and parathyroids of uraemic animals was significantly higher, while the receptor sedimentation constant (S), DNA affinity and KD were all unchanged. The ratio of occupied to total receptors was not significantly altered. The regulation of 1,25(OH)2D3 receptors in response to acute injection of 1,25(OH)2D3 was abnormal. Calbindin-D9k concentration in the intestines of uraemic and control rats was comparable both before and after administration of 1,25(OH)2D3. The present data demonstrate (a) increased 1,25(OH)2D3 receptors and (b) unchanged 1,25(OH)2D3-dependent synthesis of calcium binding protein (CaBP) in experimental uraemia.
dc.relation.ispartof urn:issn:0014-2972
dc.title No decrease of 1,25(OH)2D3 receptors and duodenal calbindin-D9k in uraemic rats.
dc.type Journal Article 2018-02-07T07:40:04Z
dc.language.rfc3066 en
dc.identifier.mtmt 1637755
dc.identifier.wos A1991GK00300011
dc.identifier.pubmed 1661239
dc.contributor.department SE/AOK/K/II. Sz. Gyermekgyógyászati Klinika
dc.contributor.institution Semmelweis Egyetem

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