Bone Growth and Turnover in Progesterone Receptor Knockout Mice
The role of progesterone receptor (PR) signaling in skeletal metabolism is controversial. To address whether signaling through the PR is necessary for normal bone growth and turnover, we performed histomorphometric and microcomputed tomography analyses of bone from homozygous female PR knockout (PRK...
Gespeichert in:
| Veröffentlicht in: | Endocrinology (Philadelphia) 2008-05, Vol.149 (5), p.2383-2390 |
|---|---|
| Hauptverfasser: | , , , , , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 2390 |
|---|---|
| container_issue | 5 |
| container_start_page | 2383 |
| container_title | Endocrinology (Philadelphia) |
| container_volume | 149 |
| creator | Rickard, David J Iwaniec, Urszula T Evans, Glenda Hefferan, Theresa E Hunter, Jamie C Waters, Katrina M Lydon, John P O’Malley, Bert W Khosla, Sundeep Spelsberg, Thomas C Turner, Russell T |
| description | The role of progesterone receptor (PR) signaling in skeletal metabolism is controversial. To address whether signaling through the PR is necessary for normal bone growth and turnover, we performed histomorphometric and microcomputed tomography analyses of bone from homozygous female PR knockout (PRKO) mice at 6, 12, and 26 wk of age. These mice possess a null mutation of the PR locus, which blocks the gene expression of A and B isoforms of PR. Body weight gain, uterine weight gain, and tibia longitudinal bone growth were normal in PRKO mice. In contrast, total, cancellous, and cortical bone mass were increased in the humerus of 12-wk-old PRKO mice, whereas cortical and cancellous bone mass in the tibia was normal. At 26 wk of age, cancellous bone area in the proximal tibia metaphysis of PRKO mice was 153% greater than age matched wild-type mice. The improved cancellous bone balance in 6-month-old PRKO mice was associated with elevated bone formation and a tendency toward reduced osteoclast perimeter. Taken together, these findings suggest that PR signaling in mice is not essential for bone growth and turnover. However, at some skeletal sites, PR signaling attenuates the accumulation of cortical and cancellous bone mass during adolescence. |
| doi_str_mv | 10.1210/en.2007-1247 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_2329269</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><oup_id>10.1210/en.2007-1247</oup_id><sourcerecordid>3130589132</sourcerecordid><originalsourceid>FETCH-LOGICAL-c608t-5159be1f45a87c81af7125a94dcd0065c7f5bfd6caf2e3e8f3d2e9c22a22997e3</originalsourceid><addsrcrecordid>eNp1kUFv1DAQhS0EokvhxhkFIeBCij124vjSCqpSEEUgVM6W15l0XbJ2sJMi_n0dbdQCgpM18qf35s0j5DGjBwwYfY3-ACiVJQMh75AVU6IqJZP0LllRyngpAeQeeZDSZR6FEPw-2WMNyFrWsCJHb4PH4jSGn-OmML4tzqfowxXGwvniSwwXmEaMM_MVLQ5jiMVHH-z3MI3FJ2fxIbnXmT7ho-XdJ9_enZwfvy_PPp9-OH5zVtqaNmNZsUqtkXWiMo20DTOdZFAZJVrbUlpXVnbVumtrazpAjk3HW0BlAQyAUhL5Pjnc6Q7TeoutRT9G0-shuq2Jv3QwTv_5491GX4QrDRwU1CoLPN0JhDQ6nawb0W5s8B7tqJVoBBWZebGYxPBjysn11iWLfW88hinpWjEOTLIMPvsLvAz5bvkAmjNOq2YGM_VqR9kYUorY3azLqJ670-j13J2eu8v4k98j3sJLWRl4vgAmWdN30Xjr0g0HFFRWrTL3cok6Df-zLBdLviPRt8FG53GImNJtmn8ueg05y74d</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>3130589132</pqid></control><display><type>article</type><title>Bone Growth and Turnover in Progesterone Receptor Knockout Mice</title><source>MEDLINE</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>Oxford University Press Journals All Titles (1996-Current)</source><source>Alma/SFX Local Collection</source><creator>Rickard, David J ; Iwaniec, Urszula T ; Evans, Glenda ; Hefferan, Theresa E ; Hunter, Jamie C ; Waters, Katrina M ; Lydon, John P ; O’Malley, Bert W ; Khosla, Sundeep ; Spelsberg, Thomas C ; Turner, Russell T</creator><creatorcontrib>Rickard, David J ; Iwaniec, Urszula T ; Evans, Glenda ; Hefferan, Theresa E ; Hunter, Jamie C ; Waters, Katrina M ; Lydon, John P ; O’Malley, Bert W ; Khosla, Sundeep ; Spelsberg, Thomas C ; Turner, Russell T ; Pacific Northwest National Lab. (PNNL), Richland, WA (United States)</creatorcontrib><description>The role of progesterone receptor (PR) signaling in skeletal metabolism is controversial. To address whether signaling through the PR is necessary for normal bone growth and turnover, we performed histomorphometric and microcomputed tomography analyses of bone from homozygous female PR knockout (PRKO) mice at 6, 12, and 26 wk of age. These mice possess a null mutation of the PR locus, which blocks the gene expression of A and B isoforms of PR. Body weight gain, uterine weight gain, and tibia longitudinal bone growth were normal in PRKO mice. In contrast, total, cancellous, and cortical bone mass were increased in the humerus of 12-wk-old PRKO mice, whereas cortical and cancellous bone mass in the tibia was normal. At 26 wk of age, cancellous bone area in the proximal tibia metaphysis of PRKO mice was 153% greater than age matched wild-type mice. The improved cancellous bone balance in 6-month-old PRKO mice was associated with elevated bone formation and a tendency toward reduced osteoclast perimeter. Taken together, these findings suggest that PR signaling in mice is not essential for bone growth and turnover. However, at some skeletal sites, PR signaling attenuates the accumulation of cortical and cancellous bone mass during adolescence.</description><identifier>ISSN: 0013-7227</identifier><identifier>EISSN: 1945-7170</identifier><identifier>DOI: 10.1210/en.2007-1247</identifier><identifier>PMID: 18276762</identifier><identifier>CODEN: ENDOAO</identifier><language>eng</language><publisher>Bethesda, MD: Endocrine Society</publisher><subject>Age Factors ; AGING ; Animals ; BASIC BIOLOGICAL SCIENCES ; Biological and medical sciences ; Body Weight ; Body weight gain ; Bone Density - genetics ; Bone Development - genetics ; Bone Development - physiology ; Bone growth ; Bone mass ; Bone Remodeling - genetics ; Bone Remodeling - physiology ; Bone turnover ; Cancellous bone ; Computed tomography ; Cortical bone ; Diaphyses - growth & development ; Epiphyses - growth & development ; Female ; FEMALES ; Fundamental and applied biological sciences. Psychology ; Gene expression ; GENES ; Humerus ; Humerus - growth & development ; Isoforms ; METABOLISM ; Metaphysis ; MICE ; Mice, Knockout ; MUTATIONS ; Organ Size ; Osteogenesis ; PROGESTERONE ; Receptors ; Receptors, Progesterone - genetics ; Signal Transduction ; TIBIA ; Tibia - growth & development ; Uterus - anatomy & histology ; Vertebrates: endocrinology</subject><ispartof>Endocrinology (Philadelphia), 2008-05, Vol.149 (5), p.2383-2390</ispartof><rights>Copyright © 2008 by the Endocrine Society 2008</rights><rights>2008 INIST-CNRS</rights><rights>Copyright © 2008 by the Endocrine Society</rights><rights>Copyright © 2008 by The Endocrine Society 2008</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c608t-5159be1f45a87c81af7125a94dcd0065c7f5bfd6caf2e3e8f3d2e9c22a22997e3</citedby><cites>FETCH-LOGICAL-c608t-5159be1f45a87c81af7125a94dcd0065c7f5bfd6caf2e3e8f3d2e9c22a22997e3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,780,784,885,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=20291215$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/18276762$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttps://www.osti.gov/biblio/948404$$D View this record in Osti.gov$$Hfree_for_read</backlink></links><search><creatorcontrib>Rickard, David J</creatorcontrib><creatorcontrib>Iwaniec, Urszula T</creatorcontrib><creatorcontrib>Evans, Glenda</creatorcontrib><creatorcontrib>Hefferan, Theresa E</creatorcontrib><creatorcontrib>Hunter, Jamie C</creatorcontrib><creatorcontrib>Waters, Katrina M</creatorcontrib><creatorcontrib>Lydon, John P</creatorcontrib><creatorcontrib>O’Malley, Bert W</creatorcontrib><creatorcontrib>Khosla, Sundeep</creatorcontrib><creatorcontrib>Spelsberg, Thomas C</creatorcontrib><creatorcontrib>Turner, Russell T</creatorcontrib><creatorcontrib>Pacific Northwest National Lab. (PNNL), Richland, WA (United States)</creatorcontrib><title>Bone Growth and Turnover in Progesterone Receptor Knockout Mice</title><title>Endocrinology (Philadelphia)</title><addtitle>Endocrinology</addtitle><description>The role of progesterone receptor (PR) signaling in skeletal metabolism is controversial. To address whether signaling through the PR is necessary for normal bone growth and turnover, we performed histomorphometric and microcomputed tomography analyses of bone from homozygous female PR knockout (PRKO) mice at 6, 12, and 26 wk of age. These mice possess a null mutation of the PR locus, which blocks the gene expression of A and B isoforms of PR. Body weight gain, uterine weight gain, and tibia longitudinal bone growth were normal in PRKO mice. In contrast, total, cancellous, and cortical bone mass were increased in the humerus of 12-wk-old PRKO mice, whereas cortical and cancellous bone mass in the tibia was normal. At 26 wk of age, cancellous bone area in the proximal tibia metaphysis of PRKO mice was 153% greater than age matched wild-type mice. The improved cancellous bone balance in 6-month-old PRKO mice was associated with elevated bone formation and a tendency toward reduced osteoclast perimeter. Taken together, these findings suggest that PR signaling in mice is not essential for bone growth and turnover. However, at some skeletal sites, PR signaling attenuates the accumulation of cortical and cancellous bone mass during adolescence.</description><subject>Age Factors</subject><subject>AGING</subject><subject>Animals</subject><subject>BASIC BIOLOGICAL SCIENCES</subject><subject>Biological and medical sciences</subject><subject>Body Weight</subject><subject>Body weight gain</subject><subject>Bone Density - genetics</subject><subject>Bone Development - genetics</subject><subject>Bone Development - physiology</subject><subject>Bone growth</subject><subject>Bone mass</subject><subject>Bone Remodeling - genetics</subject><subject>Bone Remodeling - physiology</subject><subject>Bone turnover</subject><subject>Cancellous bone</subject><subject>Computed tomography</subject><subject>Cortical bone</subject><subject>Diaphyses - growth & development</subject><subject>Epiphyses - growth & development</subject><subject>Female</subject><subject>FEMALES</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Gene expression</subject><subject>GENES</subject><subject>Humerus</subject><subject>Humerus - growth & development</subject><subject>Isoforms</subject><subject>METABOLISM</subject><subject>Metaphysis</subject><subject>MICE</subject><subject>Mice, Knockout</subject><subject>MUTATIONS</subject><subject>Organ Size</subject><subject>Osteogenesis</subject><subject>PROGESTERONE</subject><subject>Receptors</subject><subject>Receptors, Progesterone - genetics</subject><subject>Signal Transduction</subject><subject>TIBIA</subject><subject>Tibia - growth & development</subject><subject>Uterus - anatomy & histology</subject><subject>Vertebrates: endocrinology</subject><issn>0013-7227</issn><issn>1945-7170</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2008</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kUFv1DAQhS0EokvhxhkFIeBCij124vjSCqpSEEUgVM6W15l0XbJ2sJMi_n0dbdQCgpM18qf35s0j5DGjBwwYfY3-ACiVJQMh75AVU6IqJZP0LllRyngpAeQeeZDSZR6FEPw-2WMNyFrWsCJHb4PH4jSGn-OmML4tzqfowxXGwvniSwwXmEaMM_MVLQ5jiMVHH-z3MI3FJ2fxIbnXmT7ho-XdJ9_enZwfvy_PPp9-OH5zVtqaNmNZsUqtkXWiMo20DTOdZFAZJVrbUlpXVnbVumtrazpAjk3HW0BlAQyAUhL5Pjnc6Q7TeoutRT9G0-shuq2Jv3QwTv_5491GX4QrDRwU1CoLPN0JhDQ6nawb0W5s8B7tqJVoBBWZebGYxPBjysn11iWLfW88hinpWjEOTLIMPvsLvAz5bvkAmjNOq2YGM_VqR9kYUorY3azLqJ670-j13J2eu8v4k98j3sJLWRl4vgAmWdN30Xjr0g0HFFRWrTL3cok6Df-zLBdLviPRt8FG53GImNJtmn8ueg05y74d</recordid><startdate>20080501</startdate><enddate>20080501</enddate><creator>Rickard, David J</creator><creator>Iwaniec, Urszula T</creator><creator>Evans, Glenda</creator><creator>Hefferan, Theresa E</creator><creator>Hunter, Jamie C</creator><creator>Waters, Katrina M</creator><creator>Lydon, John P</creator><creator>O’Malley, Bert W</creator><creator>Khosla, Sundeep</creator><creator>Spelsberg, Thomas C</creator><creator>Turner, Russell T</creator><general>Endocrine Society</general><general>Oxford University Press</general><general>The Endocrine Society</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QG</scope><scope>7QP</scope><scope>7QR</scope><scope>7T5</scope><scope>7TM</scope><scope>7TO</scope><scope>7U7</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>K9.</scope><scope>P64</scope><scope>7X8</scope><scope>OTOTI</scope><scope>5PM</scope></search><sort><creationdate>20080501</creationdate><title>Bone Growth and Turnover in Progesterone Receptor Knockout Mice</title><author>Rickard, David J ; Iwaniec, Urszula T ; Evans, Glenda ; Hefferan, Theresa E ; Hunter, Jamie C ; Waters, Katrina M ; Lydon, John P ; O’Malley, Bert W ; Khosla, Sundeep ; Spelsberg, Thomas C ; Turner, Russell T</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c608t-5159be1f45a87c81af7125a94dcd0065c7f5bfd6caf2e3e8f3d2e9c22a22997e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2008</creationdate><topic>Age Factors</topic><topic>AGING</topic><topic>Animals</topic><topic>BASIC BIOLOGICAL SCIENCES</topic><topic>Biological and medical sciences</topic><topic>Body Weight</topic><topic>Body weight gain</topic><topic>Bone Density - genetics</topic><topic>Bone Development - genetics</topic><topic>Bone Development - physiology</topic><topic>Bone growth</topic><topic>Bone mass</topic><topic>Bone Remodeling - genetics</topic><topic>Bone Remodeling - physiology</topic><topic>Bone turnover</topic><topic>Cancellous bone</topic><topic>Computed tomography</topic><topic>Cortical bone</topic><topic>Diaphyses - growth & development</topic><topic>Epiphyses - growth & development</topic><topic>Female</topic><topic>FEMALES</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Gene expression</topic><topic>GENES</topic><topic>Humerus</topic><topic>Humerus - growth & development</topic><topic>Isoforms</topic><topic>METABOLISM</topic><topic>Metaphysis</topic><topic>MICE</topic><topic>Mice, Knockout</topic><topic>MUTATIONS</topic><topic>Organ Size</topic><topic>Osteogenesis</topic><topic>PROGESTERONE</topic><topic>Receptors</topic><topic>Receptors, Progesterone - genetics</topic><topic>Signal Transduction</topic><topic>TIBIA</topic><topic>Tibia - growth & development</topic><topic>Uterus - anatomy & histology</topic><topic>Vertebrates: endocrinology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Rickard, David J</creatorcontrib><creatorcontrib>Iwaniec, Urszula T</creatorcontrib><creatorcontrib>Evans, Glenda</creatorcontrib><creatorcontrib>Hefferan, Theresa E</creatorcontrib><creatorcontrib>Hunter, Jamie C</creatorcontrib><creatorcontrib>Waters, Katrina M</creatorcontrib><creatorcontrib>Lydon, John P</creatorcontrib><creatorcontrib>O’Malley, Bert W</creatorcontrib><creatorcontrib>Khosla, Sundeep</creatorcontrib><creatorcontrib>Spelsberg, Thomas C</creatorcontrib><creatorcontrib>Turner, Russell T</creatorcontrib><creatorcontrib>Pacific Northwest National Lab. (PNNL), Richland, WA (United States)</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Animal Behavior Abstracts</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Immunology Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><collection>OSTI.GOV</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Endocrinology (Philadelphia)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Rickard, David J</au><au>Iwaniec, Urszula T</au><au>Evans, Glenda</au><au>Hefferan, Theresa E</au><au>Hunter, Jamie C</au><au>Waters, Katrina M</au><au>Lydon, John P</au><au>O’Malley, Bert W</au><au>Khosla, Sundeep</au><au>Spelsberg, Thomas C</au><au>Turner, Russell T</au><aucorp>Pacific Northwest National Lab. (PNNL), Richland, WA (United States)</aucorp><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Bone Growth and Turnover in Progesterone Receptor Knockout Mice</atitle><jtitle>Endocrinology (Philadelphia)</jtitle><addtitle>Endocrinology</addtitle><date>2008-05-01</date><risdate>2008</risdate><volume>149</volume><issue>5</issue><spage>2383</spage><epage>2390</epage><pages>2383-2390</pages><issn>0013-7227</issn><eissn>1945-7170</eissn><coden>ENDOAO</coden><abstract>The role of progesterone receptor (PR) signaling in skeletal metabolism is controversial. To address whether signaling through the PR is necessary for normal bone growth and turnover, we performed histomorphometric and microcomputed tomography analyses of bone from homozygous female PR knockout (PRKO) mice at 6, 12, and 26 wk of age. These mice possess a null mutation of the PR locus, which blocks the gene expression of A and B isoforms of PR. Body weight gain, uterine weight gain, and tibia longitudinal bone growth were normal in PRKO mice. In contrast, total, cancellous, and cortical bone mass were increased in the humerus of 12-wk-old PRKO mice, whereas cortical and cancellous bone mass in the tibia was normal. At 26 wk of age, cancellous bone area in the proximal tibia metaphysis of PRKO mice was 153% greater than age matched wild-type mice. The improved cancellous bone balance in 6-month-old PRKO mice was associated with elevated bone formation and a tendency toward reduced osteoclast perimeter. Taken together, these findings suggest that PR signaling in mice is not essential for bone growth and turnover. However, at some skeletal sites, PR signaling attenuates the accumulation of cortical and cancellous bone mass during adolescence.</abstract><cop>Bethesda, MD</cop><pub>Endocrine Society</pub><pmid>18276762</pmid><doi>10.1210/en.2007-1247</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0013-7227 |
| ispartof | Endocrinology (Philadelphia), 2008-05, Vol.149 (5), p.2383-2390 |
| issn | 0013-7227 1945-7170 |
| language | eng |
| recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_2329269 |
| source | MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Oxford University Press Journals All Titles (1996-Current); Alma/SFX Local Collection |
| subjects | Age Factors AGING Animals BASIC BIOLOGICAL SCIENCES Biological and medical sciences Body Weight Body weight gain Bone Density - genetics Bone Development - genetics Bone Development - physiology Bone growth Bone mass Bone Remodeling - genetics Bone Remodeling - physiology Bone turnover Cancellous bone Computed tomography Cortical bone Diaphyses - growth & development Epiphyses - growth & development Female FEMALES Fundamental and applied biological sciences. Psychology Gene expression GENES Humerus Humerus - growth & development Isoforms METABOLISM Metaphysis MICE Mice, Knockout MUTATIONS Organ Size Osteogenesis PROGESTERONE Receptors Receptors, Progesterone - genetics Signal Transduction TIBIA Tibia - growth & development Uterus - anatomy & histology Vertebrates: endocrinology |
| title | Bone Growth and Turnover in Progesterone Receptor Knockout Mice |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-29T17%3A58%3A18IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Bone%20Growth%20and%20Turnover%20in%20Progesterone%20Receptor%20Knockout%20Mice&rft.jtitle=Endocrinology%20(Philadelphia)&rft.au=Rickard,%20David%20J&rft.aucorp=Pacific%20Northwest%20National%20Lab.%20(PNNL),%20Richland,%20WA%20(United%20States)&rft.date=2008-05-01&rft.volume=149&rft.issue=5&rft.spage=2383&rft.epage=2390&rft.pages=2383-2390&rft.issn=0013-7227&rft.eissn=1945-7170&rft.coden=ENDOAO&rft_id=info:doi/10.1210/en.2007-1247&rft_dat=%3Cproquest_pubme%3E3130589132%3C/proquest_pubme%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=3130589132&rft_id=info:pmid/18276762&rft_oup_id=10.1210/en.2007-1247&rfr_iscdi=true |