Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2004-2-18
pubmed:abstractText
Amylin is a member of the calcitonin family of hormones cosecreted with insulin by pancreatic beta cells. Cell culture assays suggest that amylin could affect bone formation and bone resorption, this latter function after its binding to the calcitonin receptor (CALCR). Here we show that Amylin inactivation leads to a low bone mass due to an increase in bone resorption, whereas bone formation is unaffected. In vitro, amylin inhibits fusion of mononucleated osteoclast precursors into multinucleated osteoclasts in an ERK1/2-dependent manner. Although Amylin +/- mice like Amylin-deficient mice display a low bone mass phenotype and increased bone resorption, Calcr +/- mice display a high bone mass due to an increase in bone formation. Moreover, compound heterozygote mice for Calcr and Amylin inactivation displayed bone abnormalities observed in both Calcr +/- and Amylin +/- mice, thereby ruling out that amylin uses CALCR to inhibit osteoclastogenesis in vivo. Thus, amylin is a physiological regulator of bone resorption that acts through an unidentified receptor.
pubmed:grant
pubmed:commentsCorrections
http://linkedlifedata.com/resource/pubmed/commentcorrection/14970190-10385705, http://linkedlifedata.com/resource/pubmed/commentcorrection/14970190-10423015, http://linkedlifedata.com/resource/pubmed/commentcorrection/14970190-10457262, http://linkedlifedata.com/resource/pubmed/commentcorrection/14970190-11309373, http://linkedlifedata.com/resource/pubmed/commentcorrection/14970190-11502478, http://linkedlifedata.com/resource/pubmed/commentcorrection/14970190-11823456, http://linkedlifedata.com/resource/pubmed/commentcorrection/14970190-1244549, http://linkedlifedata.com/resource/pubmed/commentcorrection/14970190-12488435, http://linkedlifedata.com/resource/pubmed/commentcorrection/14970190-12556539, http://linkedlifedata.com/resource/pubmed/commentcorrection/14970190-12748652, http://linkedlifedata.com/resource/pubmed/commentcorrection/14970190-12897775, http://linkedlifedata.com/resource/pubmed/commentcorrection/14970190-1324163, http://linkedlifedata.com/resource/pubmed/commentcorrection/14970190-2185112, http://linkedlifedata.com/resource/pubmed/commentcorrection/14970190-3016026, http://linkedlifedata.com/resource/pubmed/commentcorrection/14970190-3296768, http://linkedlifedata.com/resource/pubmed/commentcorrection/14970190-3455637, http://linkedlifedata.com/resource/pubmed/commentcorrection/14970190-7664679, http://linkedlifedata.com/resource/pubmed/commentcorrection/14970190-8311941, http://linkedlifedata.com/resource/pubmed/commentcorrection/14970190-9209829, http://linkedlifedata.com/resource/pubmed/commentcorrection/14970190-9330291, http://linkedlifedata.com/resource/pubmed/commentcorrection/14970190-9677414, http://linkedlifedata.com/resource/pubmed/commentcorrection/14970190-9753619, http://linkedlifedata.com/resource/pubmed/commentcorrection/14970190-9755090
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0021-9525
pubmed:author
pubmed:copyrightInfo
Copyright The Rockefeller University Press
pubmed:issnType
Print
pubmed:day
16
pubmed:volume
164
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
509-14
pubmed:dateRevised
2010-11-18
pubmed:meshHeading
pubmed:year
2004
pubmed:articleTitle
Amylin inhibits bone resorption while the calcitonin receptor controls bone formation in vivo.
pubmed:affiliation
Department of Molecular and Human Genetics and Bone Disease Program of Texas, Baylor College of Medicine, One Baylor Plaza, Room S921, Houston, TX 77030, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, U.S. Gov't, Non-P.H.S., Research Support, Non-U.S. Gov't