Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
12
pubmed:dateCreated
1998-7-14
pubmed:abstractText
The calcium-sensing receptor (CaSR) regulates PTH secretion to control the extracellular calcium concentration in adults, but its role in fetal life is unknown. We used CaSR gene knockout mice to investigate the role of the CaSR in regulating fetal calcium metabolism. The normal calcium concentration in fetal blood is raised above the maternal level, an increase that depends upon PTH-related peptide (PTHrP). Heterozygous (+/-) and homozygous (-/-) disruption of the CaSR caused a further increase in the fetal calcium level. This increase was modestly blunted by concomitant disruption of the PTHrP gene and completely reversed by disruption of the PTH/ PTHrP receptor gene. Serum levels of PTH and 1, 25-dihydroxyvitamin D were substantially increased above the normal low fetal levels by disruption of the CaSR. The free deoxypyridinoline level was increased in the amniotic fluid (urine) of CaSR-/- fetuses; this result suggests that fetal bone resorption is increased. Placental calcium transfer was reduced, and renal calcium excretion was increased, by disruption of the CaSR. These studies indicate that the CaSR normally suppresses PTH secretion in the presence of the normal raised (and PTHrP-dependent) fetal calcium level. Disruption of the CaSR causes fetal hyperparathyroidism and hypercalcemia, with additional effects on placental calcium transfer.
pubmed:grant
pubmed:commentsCorrections
http://linkedlifedata.com/resource/pubmed/commentcorrection/9637715-1731634, http://linkedlifedata.com/resource/pubmed/commentcorrection/9637715-2223059, http://linkedlifedata.com/resource/pubmed/commentcorrection/9637715-2232895, http://linkedlifedata.com/resource/pubmed/commentcorrection/9637715-2798763, http://linkedlifedata.com/resource/pubmed/commentcorrection/9637715-3786294, http://linkedlifedata.com/resource/pubmed/commentcorrection/9637715-4203705, http://linkedlifedata.com/resource/pubmed/commentcorrection/9637715-4625420, http://linkedlifedata.com/resource/pubmed/commentcorrection/9637715-6622431, http://linkedlifedata.com/resource/pubmed/commentcorrection/9637715-6715720, http://linkedlifedata.com/resource/pubmed/commentcorrection/9637715-6720905, http://linkedlifedata.com/resource/pubmed/commentcorrection/9637715-7493018, http://linkedlifedata.com/resource/pubmed/commentcorrection/9637715-7581942, http://linkedlifedata.com/resource/pubmed/commentcorrection/9637715-7588259, http://linkedlifedata.com/resource/pubmed/commentcorrection/9637715-7724534, http://linkedlifedata.com/resource/pubmed/commentcorrection/9637715-7791841, http://linkedlifedata.com/resource/pubmed/commentcorrection/9637715-7816802, http://linkedlifedata.com/resource/pubmed/commentcorrection/9637715-7874174, http://linkedlifedata.com/resource/pubmed/commentcorrection/9637715-7916660, http://linkedlifedata.com/resource/pubmed/commentcorrection/9637715-8148666, http://linkedlifedata.com/resource/pubmed/commentcorrection/9637715-8255296, http://linkedlifedata.com/resource/pubmed/commentcorrection/9637715-8314082, http://linkedlifedata.com/resource/pubmed/commentcorrection/9637715-8662561, http://linkedlifedata.com/resource/pubmed/commentcorrection/9637715-8813042, http://linkedlifedata.com/resource/pubmed/commentcorrection/9637715-8853437, http://linkedlifedata.com/resource/pubmed/commentcorrection/9637715-8854047, http://linkedlifedata.com/resource/pubmed/commentcorrection/9637715-8938590, http://linkedlifedata.com/resource/pubmed/commentcorrection/9637715-8986793, http://linkedlifedata.com/resource/pubmed/commentcorrection/9637715-9408745
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0021-9738
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
101
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2812-20
pubmed:dateRevised
2009-11-18
pubmed:meshHeading
pubmed:year
1998
pubmed:articleTitle
Regulation of murine fetal-placental calcium metabolism by the calcium-sensing receptor.
pubmed:affiliation
Endocrine Unit, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts 02114, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't