Glucose metabolic abnormality is associated with defective mineral homeostasis in skeletal disorder mouse model
Bone was reported as a crucial organ for regulating glucose homeostasis. In this study, we found that Phex mutant mice （PUG）, a model of human X-linked hypophosphatemic rickets （XLH）, displayed metabolic abnormality in addition to abnormal phosphate homeostasis, skeletal deformity and growth retarda...
Gespeichert in:
| Veröffentlicht in: | Science China. Life sciences 2015-04, Vol.58 (4), p.359-367 |
|---|---|
| Hauptverfasser: | , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 367 |
|---|---|
| container_issue | 4 |
| container_start_page | 359 |
| container_title | Science China. Life sciences |
| container_volume | 58 |
| creator | Zou, JiangHuan Xiong, XiWen Lai, BeiBei Sun, Min Tu, Xin Gao, Xiang |
| description | Bone was reported as a crucial organ for regulating glucose homeostasis. In this study, we found that Phex mutant mice （PUG）, a model of human X-linked hypophosphatemic rickets （XLH）, displayed metabolic abnormality in addition to abnormal phosphate homeostasis, skeletal deformity and growth retardation. Glucose tolerance was elevated with enhanced insulin sensitivity in PUG, though circulating insulin level decreased. Interestingly, bone mineral density defects and glucose metabolic abnormality were both rescued by adding phosphorus- and calcium-enriched supplements in daily diet. Serum insulin level, glucose tolerance and insulin sensitivity showed no differences between PUG and wild-type mice with rescued osteocalcin （OCN） following treatment. Our study suggested that OCN is a potential mediator between mineral homeostasis and glucose metabolism. This investigation brings a new perspective on glucose metabolism regulation through skeleton triggered mineral homeostasis and provides new clues in clinical therapeutics of potential metabolic disorders in XLH patients. |
| doi_str_mv | 10.1007/s11427-015-4827-2 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_1676348699</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><cqvip_id>664263290</cqvip_id><sourcerecordid>1672608604</sourcerecordid><originalsourceid>FETCH-LOGICAL-c475t-63d15a99a3c63de843dac268fc7619b9f61168ab331fb24879622989767f51633</originalsourceid><addsrcrecordid>eNqNkUtv1TAQhS0EolXpD2CDLNiwCfgVP5aogoJUiQ2sLceZ9Lo4cWsnoP575nIvFWKB8MYj-TtnxnMIec7ZG86Yeds4V8J0jPedsliIR-SUW-06bq17jLU2qjOS9SfkvLUbhkdKJox5Sk5Eb7XQvTsl5TJvsTSgM6xhKDlFGoal1DnktN7T1GhorcQUVhjpj7Tu6AgTxDV9R0laoIZMd2WG0tbQkE4Lbd8go1mmY2qljlDpXLZ9hzJCfkaeTCE3OD_eZ-Trh_dfLj52V58vP128u-qiMv3aaTnyPjgXZMQSrJJjiELbKRrN3eAmzbm2YZCST4NQ1jgthLPOaDP1XEt5Rl4ffG9rudugrX5OLULOYQGcxuN2tFS4Lvc_qNDMaqYQffUXelO2uuBHflFCS2YNUvxAxVpaqzD525rmUO89Z36fnT9k5zE7v8_OC9S8ODpvwwzjg-J3UgiIA9DwabmG-kfrf7i-PE6yK8v1HeoejLVWOK5wTP4E8PuvGQ</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1672263087</pqid></control><display><type>article</type><title>Glucose metabolic abnormality is associated with defective mineral homeostasis in skeletal disorder mouse model</title><source>MEDLINE</source><source>Alma/SFX Local Collection</source><source>SpringerLink Journals - AutoHoldings</source><creator>Zou, JiangHuan ; Xiong, XiWen ; Lai, BeiBei ; Sun, Min ; Tu, Xin ; Gao, Xiang</creator><creatorcontrib>Zou, JiangHuan ; Xiong, XiWen ; Lai, BeiBei ; Sun, Min ; Tu, Xin ; Gao, Xiang</creatorcontrib><description>Bone was reported as a crucial organ for regulating glucose homeostasis. In this study, we found that Phex mutant mice （PUG）, a model of human X-linked hypophosphatemic rickets （XLH）, displayed metabolic abnormality in addition to abnormal phosphate homeostasis, skeletal deformity and growth retardation. Glucose tolerance was elevated with enhanced insulin sensitivity in PUG, though circulating insulin level decreased. Interestingly, bone mineral density defects and glucose metabolic abnormality were both rescued by adding phosphorus- and calcium-enriched supplements in daily diet. Serum insulin level, glucose tolerance and insulin sensitivity showed no differences between PUG and wild-type mice with rescued osteocalcin （OCN） following treatment. Our study suggested that OCN is a potential mediator between mineral homeostasis and glucose metabolism. This investigation brings a new perspective on glucose metabolism regulation through skeleton triggered mineral homeostasis and provides new clues in clinical therapeutics of potential metabolic disorders in XLH patients.</description><identifier>ISSN: 1674-7305</identifier><identifier>EISSN: 1869-1889</identifier><identifier>DOI: 10.1007/s11427-015-4827-2</identifier><identifier>PMID: 25862659</identifier><language>eng</language><publisher>Beijing: Science China Press</publisher><subject>Animals ; Biomedical and Life Sciences ; Bone Diseases - metabolism ; Disease Models, Animal ; Familial Hypophosphatemic Rickets - diet therapy ; Familial Hypophosphatemic Rickets - genetics ; Familial Hypophosphatemic Rickets - metabolism ; Glucose - metabolism ; Homeostasis ; Life Sciences ; Mice ; Mice, Mutant Strains ; Minerals - metabolism ; PHEX Phosphate Regulating Neutral Endopeptidase - genetics ; Research Paper ; 临床治疗 ; 代谢异常 ; 小鼠模型 ; 物质平衡 ; 缺陷 ; 胰岛素敏感性 ; 葡萄糖 ; 骨骼疾病</subject><ispartof>Science China. Life sciences, 2015-04, Vol.58 (4), p.359-367</ispartof><rights>The Author(s) 2015. This article is published under license to BioMed Central Ltd. This article is distributed under the terms of the Creative Commons Attribution License which permits any use, distribution, and reproduction in any medium, provided the original author(s) and source are credited.</rights><rights>Science in China Press and Springer-Verlag GmbH 2015</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c475t-63d15a99a3c63de843dac268fc7619b9f61168ab331fb24879622989767f51633</citedby><cites>FETCH-LOGICAL-c475t-63d15a99a3c63de843dac268fc7619b9f61168ab331fb24879622989767f51633</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Uhttp://image.cqvip.com/vip1000/qk/60112X/60112X.jpg</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s11427-015-4827-2$$EPDF$$P50$$Gspringer$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s11427-015-4827-2$$EHTML$$P50$$Gspringer$$Hfree_for_read</linktohtml><link.rule.ids>314,776,780,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25862659$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zou, JiangHuan</creatorcontrib><creatorcontrib>Xiong, XiWen</creatorcontrib><creatorcontrib>Lai, BeiBei</creatorcontrib><creatorcontrib>Sun, Min</creatorcontrib><creatorcontrib>Tu, Xin</creatorcontrib><creatorcontrib>Gao, Xiang</creatorcontrib><title>Glucose metabolic abnormality is associated with defective mineral homeostasis in skeletal disorder mouse model</title><title>Science China. Life sciences</title><addtitle>Sci. China Life Sci</addtitle><addtitle>Sci China Life Sci</addtitle><description>Bone was reported as a crucial organ for regulating glucose homeostasis. In this study, we found that Phex mutant mice （PUG）, a model of human X-linked hypophosphatemic rickets （XLH）, displayed metabolic abnormality in addition to abnormal phosphate homeostasis, skeletal deformity and growth retardation. Glucose tolerance was elevated with enhanced insulin sensitivity in PUG, though circulating insulin level decreased. Interestingly, bone mineral density defects and glucose metabolic abnormality were both rescued by adding phosphorus- and calcium-enriched supplements in daily diet. Serum insulin level, glucose tolerance and insulin sensitivity showed no differences between PUG and wild-type mice with rescued osteocalcin （OCN） following treatment. Our study suggested that OCN is a potential mediator between mineral homeostasis and glucose metabolism. This investigation brings a new perspective on glucose metabolism regulation through skeleton triggered mineral homeostasis and provides new clues in clinical therapeutics of potential metabolic disorders in XLH patients.</description><subject>Animals</subject><subject>Biomedical and Life Sciences</subject><subject>Bone Diseases - metabolism</subject><subject>Disease Models, Animal</subject><subject>Familial Hypophosphatemic Rickets - diet therapy</subject><subject>Familial Hypophosphatemic Rickets - genetics</subject><subject>Familial Hypophosphatemic Rickets - metabolism</subject><subject>Glucose - metabolism</subject><subject>Homeostasis</subject><subject>Life Sciences</subject><subject>Mice</subject><subject>Mice, Mutant Strains</subject><subject>Minerals - metabolism</subject><subject>PHEX Phosphate Regulating Neutral Endopeptidase - genetics</subject><subject>Research Paper</subject><subject>临床治疗</subject><subject>代谢异常</subject><subject>小鼠模型</subject><subject>物质平衡</subject><subject>缺陷</subject><subject>胰岛素敏感性</subject><subject>葡萄糖</subject><subject>骨骼疾病</subject><issn>1674-7305</issn><issn>1869-1889</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>C6C</sourceid><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNqNkUtv1TAQhS0EolXpD2CDLNiwCfgVP5aogoJUiQ2sLceZ9Lo4cWsnoP575nIvFWKB8MYj-TtnxnMIec7ZG86Yeds4V8J0jPedsliIR-SUW-06bq17jLU2qjOS9SfkvLUbhkdKJox5Sk5Eb7XQvTsl5TJvsTSgM6xhKDlFGoal1DnktN7T1GhorcQUVhjpj7Tu6AgTxDV9R0laoIZMd2WG0tbQkE4Lbd8go1mmY2qljlDpXLZ9hzJCfkaeTCE3OD_eZ-Trh_dfLj52V58vP128u-qiMv3aaTnyPjgXZMQSrJJjiELbKRrN3eAmzbm2YZCST4NQ1jgthLPOaDP1XEt5Rl4ffG9rudugrX5OLULOYQGcxuN2tFS4Lvc_qNDMaqYQffUXelO2uuBHflFCS2YNUvxAxVpaqzD525rmUO89Z36fnT9k5zE7v8_OC9S8ODpvwwzjg-J3UgiIA9DwabmG-kfrf7i-PE6yK8v1HeoejLVWOK5wTP4E8PuvGQ</recordid><startdate>20150401</startdate><enddate>20150401</enddate><creator>Zou, JiangHuan</creator><creator>Xiong, XiWen</creator><creator>Lai, BeiBei</creator><creator>Sun, Min</creator><creator>Tu, Xin</creator><creator>Gao, Xiang</creator><general>Science China Press</general><general>Springer Nature B.V</general><scope>2RA</scope><scope>92L</scope><scope>CQIGP</scope><scope>~WA</scope><scope>C6C</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>3V.</scope><scope>7QP</scope><scope>7TK</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>8AO</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope></search><sort><creationdate>20150401</creationdate><title>Glucose metabolic abnormality is associated with defective mineral homeostasis in skeletal disorder mouse model</title><author>Zou, JiangHuan ; Xiong, XiWen ; Lai, BeiBei ; Sun, Min ; Tu, Xin ; Gao, Xiang</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c475t-63d15a99a3c63de843dac268fc7619b9f61168ab331fb24879622989767f51633</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Animals</topic><topic>Biomedical and Life Sciences</topic><topic>Bone Diseases - metabolism</topic><topic>Disease Models, Animal</topic><topic>Familial Hypophosphatemic Rickets - diet therapy</topic><topic>Familial Hypophosphatemic Rickets - genetics</topic><topic>Familial Hypophosphatemic Rickets - metabolism</topic><topic>Glucose - metabolism</topic><topic>Homeostasis</topic><topic>Life Sciences</topic><topic>Mice</topic><topic>Mice, Mutant Strains</topic><topic>Minerals - metabolism</topic><topic>PHEX Phosphate Regulating Neutral Endopeptidase - genetics</topic><topic>Research Paper</topic><topic>临床治疗</topic><topic>代谢异常</topic><topic>小鼠模型</topic><topic>物质平衡</topic><topic>缺陷</topic><topic>胰岛素敏感性</topic><topic>葡萄糖</topic><topic>骨骼疾病</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zou, JiangHuan</creatorcontrib><creatorcontrib>Xiong, XiWen</creatorcontrib><creatorcontrib>Lai, BeiBei</creatorcontrib><creatorcontrib>Sun, Min</creatorcontrib><creatorcontrib>Tu, Xin</creatorcontrib><creatorcontrib>Gao, Xiang</creatorcontrib><collection>中文科技期刊数据库</collection><collection>中文科技期刊数据库-CALIS站点</collection><collection>中文科技期刊数据库-7.0平台</collection><collection>中文科技期刊数据库- 镜像站点</collection><collection>Springer Nature OA Free Journals</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biological Science Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><jtitle>Science China. Life sciences</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zou, JiangHuan</au><au>Xiong, XiWen</au><au>Lai, BeiBei</au><au>Sun, Min</au><au>Tu, Xin</au><au>Gao, Xiang</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Glucose metabolic abnormality is associated with defective mineral homeostasis in skeletal disorder mouse model</atitle><jtitle>Science China. Life sciences</jtitle><stitle>Sci. China Life Sci</stitle><addtitle>Sci China Life Sci</addtitle><date>2015-04-01</date><risdate>2015</risdate><volume>58</volume><issue>4</issue><spage>359</spage><epage>367</epage><pages>359-367</pages><issn>1674-7305</issn><eissn>1869-1889</eissn><abstract>Bone was reported as a crucial organ for regulating glucose homeostasis. In this study, we found that Phex mutant mice （PUG）, a model of human X-linked hypophosphatemic rickets （XLH）, displayed metabolic abnormality in addition to abnormal phosphate homeostasis, skeletal deformity and growth retardation. Glucose tolerance was elevated with enhanced insulin sensitivity in PUG, though circulating insulin level decreased. Interestingly, bone mineral density defects and glucose metabolic abnormality were both rescued by adding phosphorus- and calcium-enriched supplements in daily diet. Serum insulin level, glucose tolerance and insulin sensitivity showed no differences between PUG and wild-type mice with rescued osteocalcin （OCN） following treatment. Our study suggested that OCN is a potential mediator between mineral homeostasis and glucose metabolism. This investigation brings a new perspective on glucose metabolism regulation through skeleton triggered mineral homeostasis and provides new clues in clinical therapeutics of potential metabolic disorders in XLH patients.</abstract><cop>Beijing</cop><pub>Science China Press</pub><pmid>25862659</pmid><doi>10.1007/s11427-015-4827-2</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1674-7305 |
| ispartof | Science China. Life sciences, 2015-04, Vol.58 (4), p.359-367 |
| issn | 1674-7305 1869-1889 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_1676348699 |
| source | MEDLINE; Alma/SFX Local Collection; SpringerLink Journals - AutoHoldings |
| subjects | Animals Biomedical and Life Sciences Bone Diseases - metabolism Disease Models, Animal Familial Hypophosphatemic Rickets - diet therapy Familial Hypophosphatemic Rickets - genetics Familial Hypophosphatemic Rickets - metabolism Glucose - metabolism Homeostasis Life Sciences Mice Mice, Mutant Strains Minerals - metabolism PHEX Phosphate Regulating Neutral Endopeptidase - genetics Research Paper 临床治疗 代谢异常 小鼠模型 物质平衡 缺陷 胰岛素敏感性 葡萄糖 骨骼疾病 |
| title | Glucose metabolic abnormality is associated with defective mineral homeostasis in skeletal disorder mouse model |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-03T17%3A16%3A45IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Glucose%20metabolic%20abnormality%20is%20associated%20with%20defective%20mineral%20homeostasis%20in%20skeletal%20disorder%20mouse%20model&rft.jtitle=Science%20China.%20Life%20sciences&rft.au=Zou,%20JiangHuan&rft.date=2015-04-01&rft.volume=58&rft.issue=4&rft.spage=359&rft.epage=367&rft.pages=359-367&rft.issn=1674-7305&rft.eissn=1869-1889&rft_id=info:doi/10.1007/s11427-015-4827-2&rft_dat=%3Cproquest_cross%3E1672608604%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1672263087&rft_id=info:pmid/25862659&rft_cqvip_id=664263290&rfr_iscdi=true |