Effects of insulin-like growth factor I on the development of osteoblasts in hyperglycemia.
Identifieur interne : 000434 ( Main/Exploration ); précédent : 000433; suivant : 000435Effects of insulin-like growth factor I on the development of osteoblasts in hyperglycemia.
Auteurs : Ying Fang [République populaire de Chine] ; Zhong-Yi Wang ; Yong Mao ; Hai-Tao Xin ; Guang-Li Ren ; Xue-Fan BaiSource :
- Diabetes research and clinical practice [ 0168-8227 ] ; 2006.
Descripteurs français
- KwdFr :
- Animaux (MeSH), Calcium (métabolisme), Cellules cultivées (MeSH), Facteur de croissance IGF-I (pharmacologie), Hyperglycémie (anatomopathologie), Insuline (pharmacologie), Ostéoblastes (cytologie), Ostéoblastes (effets des médicaments et des substances chimiques), Rats (MeSH), Transporteur de glucose de type 1 (biosynthèse).
- MESH :
- anatomopathologie : Hyperglycémie.
- biosynthèse : Transporteur de glucose de type 1.
- cytologie : Ostéoblastes.
- effets des médicaments et des substances chimiques : Ostéoblastes.
- métabolisme : Calcium.
- pharmacologie : Facteur de croissance IGF-I, Insuline.
- Animaux, Cellules cultivées, Rats.
English descriptors
- KwdEn :
- MESH :
- chemical , biosynthesis : Glucose Transporter Type 1.
- chemical , metabolism : Calcium.
- cytology : Osteoblasts.
- drug effects : Osteoblasts.
- pathology : Hyperglycemia.
- chemical , pharmacology : Insulin, Insulin-Like Growth Factor I.
- Animals, Cells, Cultured, Rats.
Abstract
The delayed wound healing of tooth extraction, the activation of alveolar absorption and the being hindered bone formation around the implants in diabetes are difficult to be solved for dentists. So, the aim of the study was to investigate the influences of hyperglycemia and insulin-like growth factor I (IGF-I) on osteoblasts. Osteoblasts were cultured in different conditions: normal glucose, mimic hyperglycemia, hyperglycemia with IGF-I, hyperglycemia with insulin. The proliferation and mineralization of osteoblasts were observed. As abnormal transport of glucose involved in the development of chronic complications in diabetes. The expression of glucose transporter 1 (GLUT1) was further evaluated by RT-PCR, immunofluorescence and Western blot in different groups. These results showed that hyperglycemia increased the proliferation and inhibited the mineralization of osteoblasts, while IGF-I seemed to reverse these effects. The levels of GLUT1 mRNA and protein in hyperglycemia were elevated by 51% and 35%, respectively, compared with that in normal glucose, while the levels in hyperglycemia with IGF-I were almost the same as that in normal glucose. In conclusion, the increased expression of GLUT1 may contribute to the delayed mineralization of osteoblasts in hyperglycemia. Also IGF-I may be a new drug for diabetic bone disease through normalizing the expression of GLUT1.
DOI: 10.1016/j.diabres.2005.11.010
PubMed: 16413942
Affiliations:
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sortKey="Mao, Yong" sort="Mao, Yong" uniqKey="Mao Y" first="Yong" last="Mao">Yong Mao</name></author><author><name sortKey="Xin, Hai Tao" sort="Xin, Hai Tao" uniqKey="Xin H" first="Hai-Tao" last="Xin">Hai-Tao Xin</name></author><author><name sortKey="Ren, Guang Li" sort="Ren, Guang Li" uniqKey="Ren G" first="Guang-Li" last="Ren">Guang-Li Ren</name></author><author><name sortKey="Bai, Xue Fan" sort="Bai, Xue Fan" uniqKey="Bai X" first="Xue-Fan" last="Bai">Xue-Fan Bai</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2006">2006</date><idno type="RBID">pubmed:16413942</idno><idno type="pmid">16413942</idno><idno type="doi">10.1016/j.diabres.2005.11.010</idno><idno type="wicri:Area/Main/Corpus">000443</idno><idno type="wicri:explorRef" wicri:stream="Main" wicri:step="Corpus" wicri:corpus="PubMed">000443</idno><idno type="wicri:Area/Main/Curation">000443</idno><idno type="wicri:explorRef" wicri:stream="Main" 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Zhong Yi" uniqKey="Wang Z" first="Zhong-Yi" last="Wang">Zhong-Yi Wang</name></author><author><name sortKey="Mao, Yong" sort="Mao, Yong" uniqKey="Mao Y" first="Yong" last="Mao">Yong Mao</name></author><author><name sortKey="Xin, Hai Tao" sort="Xin, Hai Tao" uniqKey="Xin H" first="Hai-Tao" last="Xin">Hai-Tao Xin</name></author><author><name sortKey="Ren, Guang Li" sort="Ren, Guang Li" uniqKey="Ren G" first="Guang-Li" last="Ren">Guang-Li Ren</name></author><author><name sortKey="Bai, Xue Fan" sort="Bai, Xue Fan" uniqKey="Bai X" first="Xue-Fan" last="Bai">Xue-Fan Bai</name></author></analytic><series><title level="j">Diabetes research and clinical practice</title><idno type="ISSN">0168-8227</idno><imprint><date when="2006" type="published">2006</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals (MeSH)</term><term>Calcium (metabolism)</term><term>Cells, Cultured (MeSH)</term><term>Glucose Transporter Type 1 (biosynthesis)</term><term>Hyperglycemia (pathology)</term><term>Insulin (pharmacology)</term><term>Insulin-Like Growth Factor I (pharmacology)</term><term>Osteoblasts (cytology)</term><term>Osteoblasts (drug effects)</term><term>Rats (MeSH)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Animaux (MeSH)</term><term>Calcium (métabolisme)</term><term>Cellules cultivées (MeSH)</term><term>Facteur de croissance IGF-I (pharmacologie)</term><term>Hyperglycémie (anatomopathologie)</term><term>Insuline (pharmacologie)</term><term>Ostéoblastes (cytologie)</term><term>Ostéoblastes (effets des médicaments et des substances chimiques)</term><term>Rats (MeSH)</term><term>Transporteur de glucose de type 1 (biosynthèse)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="biosynthesis" xml:lang="en"><term>Glucose Transporter Type 1</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Calcium</term></keywords><keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Hyperglycémie</term></keywords><keywords scheme="MESH" qualifier="biosynthèse" xml:lang="fr"><term>Transporteur de glucose de type 1</term></keywords><keywords scheme="MESH" qualifier="cytologie" xml:lang="fr"><term>Ostéoblastes</term></keywords><keywords scheme="MESH" qualifier="cytology" xml:lang="en"><term>Osteoblasts</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Osteoblasts</term></keywords><keywords scheme="MESH" qualifier="effets des médicaments et des substances chimiques" xml:lang="fr"><term>Ostéoblastes</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Calcium</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Hyperglycemia</term></keywords><keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Facteur de croissance IGF-I</term><term>Insuline</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Insulin</term><term>Insulin-Like Growth Factor I</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Cells, Cultured</term><term>Rats</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Cellules cultivées</term><term>Rats</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The delayed wound healing of tooth extraction, the activation of alveolar absorption and the being hindered bone formation around the implants in diabetes are difficult to be solved for dentists. So, the aim of the study was to investigate the influences of hyperglycemia and insulin-like growth factor I (IGF-I) on osteoblasts. Osteoblasts were cultured in different conditions: normal glucose, mimic hyperglycemia, hyperglycemia with IGF-I, hyperglycemia with insulin. The proliferation and mineralization of osteoblasts were observed. As abnormal transport of glucose involved in the development of chronic complications in diabetes. The expression of glucose transporter 1 (GLUT1) was further evaluated by RT-PCR, immunofluorescence and Western blot in different groups. These results showed that hyperglycemia increased the proliferation and inhibited the mineralization of osteoblasts, while IGF-I seemed to reverse these effects. The levels of GLUT1 mRNA and protein in hyperglycemia were elevated by 51% and 35%, respectively, compared with that in normal glucose, while the levels in hyperglycemia with IGF-I were almost the same as that in normal glucose. In conclusion, the increased expression of GLUT1 may contribute to the delayed mineralization of osteoblasts in hyperglycemia. Also IGF-I may be a new drug for diabetic bone disease through normalizing the expression of GLUT1.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">16413942</PMID><DateCompleted><Year>2006</Year><Month>11</Month><Day>30</Day></DateCompleted><DateRevised><Year>2013</Year><Month>11</Month><Day>21</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Print">0168-8227</ISSN><JournalIssue CitedMedium="Print"><Volume>73</Volume><Issue>1</Issue><PubDate><Year>2006</Year><Month>Jul</Month></PubDate></JournalIssue><Title>Diabetes research and clinical practice</Title><ISOAbbreviation>Diabetes Res Clin Pract</ISOAbbreviation></Journal><ArticleTitle>Effects of insulin-like growth factor I on the development of osteoblasts in hyperglycemia.</ArticleTitle><Pagination><MedlinePgn>95-7</MedlinePgn></Pagination><Abstract><AbstractText>The delayed wound healing of tooth extraction, the activation of alveolar absorption and the being hindered bone formation around the implants in diabetes are difficult to be solved for dentists. So, the aim of the study was to investigate the influences of hyperglycemia and insulin-like growth factor I (IGF-I) on osteoblasts. Osteoblasts were cultured in different conditions: normal glucose, mimic hyperglycemia, hyperglycemia with IGF-I, hyperglycemia with insulin. The proliferation and mineralization of osteoblasts were observed. As abnormal transport of glucose involved in the development of chronic complications in diabetes. The expression of glucose transporter 1 (GLUT1) was further evaluated by RT-PCR, immunofluorescence and Western blot in different groups. These results showed that hyperglycemia increased the proliferation and inhibited the mineralization of osteoblasts, while IGF-I seemed to reverse these effects. The levels of GLUT1 mRNA and protein in hyperglycemia were elevated by 51% and 35%, respectively, compared with that in normal glucose, while the levels in hyperglycemia with IGF-I were almost the same as that in normal glucose. In conclusion, the increased expression of GLUT1 may contribute to the delayed mineralization of osteoblasts in hyperglycemia. Also IGF-I may be a new drug for diabetic bone disease through normalizing the expression of GLUT1.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Fang</LastName><ForeName>Ying</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Department of Prosthodontics, College of Stomatology, Fourth Military Medical University, ChangLeXi Road, XinCheng District, Xi'an 710032, Shan-Xi province, China. fangying@fmmu.edu.cn</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wang</LastName><ForeName>Zhong-Yi</ForeName><Initials>ZY</Initials></Author><Author ValidYN="Y"><LastName>Mao</LastName><ForeName>Yong</ForeName><Initials>Y</Initials></Author><Author ValidYN="Y"><LastName>Xin</LastName><ForeName>Hai-Tao</ForeName><Initials>HT</Initials></Author><Author ValidYN="Y"><LastName>Ren</LastName><ForeName>Guang-Li</ForeName><Initials>GL</Initials></Author><Author ValidYN="Y"><LastName>Bai</LastName><ForeName>Xue-Fan</ForeName><Initials>XF</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2006</Year><Month>01</Month><Day>18</Day></ArticleDate></Article><MedlineJournalInfo><Country>Ireland</Country><MedlineTA>Diabetes Res Clin Pract</MedlineTA><NlmUniqueID>8508335</NlmUniqueID><ISSNLinking>0168-8227</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D051272">Glucose Transporter Type 1</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D007328">Insulin</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C495679">Slc2a1 protein, rat</NameOfSubstance></Chemical><Chemical><RegistryNumber>67763-96-6</RegistryNumber><NameOfSubstance UI="D007334">Insulin-Like Growth Factor I</NameOfSubstance></Chemical><Chemical><RegistryNumber>SY7Q814VUP</RegistryNumber><NameOfSubstance UI="D002118">Calcium</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002118" MajorTopicYN="N">Calcium</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002478" MajorTopicYN="N">Cells, Cultured</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D051272" MajorTopicYN="N">Glucose Transporter Type 1</DescriptorName><QualifierName UI="Q000096" MajorTopicYN="N">biosynthesis</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006943" MajorTopicYN="N">Hyperglycemia</DescriptorName><QualifierName UI="Q000473" MajorTopicYN="Y">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName 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PubStatus="pubmed"><Year>2006</Year><Month>1</Month><Day>18</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2006</Year><Month>12</Month><Day>9</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2006</Year><Month>1</Month><Day>18</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">16413942</ArticleId><ArticleId IdType="pii">S0168-8227(05)00442-0</ArticleId><ArticleId IdType="doi">10.1016/j.diabres.2005.11.010</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>République populaire de Chine</li></country></list><tree><noCountry><name sortKey="Bai, Xue Fan" sort="Bai, Xue Fan" uniqKey="Bai X" first="Xue-Fan" last="Bai">Xue-Fan Bai</name><name sortKey="Mao, Yong" sort="Mao, Yong" uniqKey="Mao Y" first="Yong" last="Mao">Yong Mao</name><name sortKey="Ren, Guang Li" sort="Ren, Guang Li" uniqKey="Ren G" first="Guang-Li" last="Ren">Guang-Li Ren</name><name sortKey="Wang, Zhong Yi" sort="Wang, Zhong Yi" uniqKey="Wang Z" first="Zhong-Yi" last="Wang">Zhong-Yi Wang</name><name sortKey="Xin, Hai Tao" sort="Xin, Hai Tao" uniqKey="Xin H" first="Hai-Tao" last="Xin">Hai-Tao Xin</name></noCountry><country name="République populaire de Chine"><noRegion><name sortKey="Fang, Ying" sort="Fang, Ying" uniqKey="Fang Y" first="Ying" last="Fang">Ying Fang</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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