Effects of periodontitis on aortic insulin resistance in an obese rat model
The combination of obesity and its associated risk factors, such as insulin resistance and inflammation, results in the development of atherosclerosis. However, the effects of periodontitis on atherosclerosis in an obese body remain unclear. The aim of the study was to investigate the effects of lig...
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creator | Ekuni, Daisuke Tomofuji, Takaaki Irie, Koichiro Kasuyama, Kenta Umakoshi, Michihiro Azuma, Tetsuji Tamaki, Naofumi Sanbe, Toshihiro Endo, Yasumasa Yamamoto, Tatsuo Nishida, Takashi Morita, Manabu |
description | The combination of obesity and its associated risk factors, such as insulin resistance and inflammation, results in the development of atherosclerosis. However, the effects of periodontitis on atherosclerosis in an obese body remain unclear. The aim of the study was to investigate the effects of ligature-induced periodontitis in Zucker fatty rats on initiation of atherosclerosis by evaluating aortic insulin resistance. Zucker fatty rats (n=24) were divided into two groups. In the periodontitis group, periodontitis was ligature-induced for 4 weeks, whereas the control group was left unligated. After the 4-week experimental period, descending aorta was used for measuring the levels of lipid deposits, immunohistochemical analysis, and evaluation of gene expression. Levels of serum C-reactive protein (CRP), tumor necrosis factor-α (TNF-α), and insulin were also measured. Rats in the periodontitis group had significantly enhanced lipid deposits in the aorta, but not in the control group. Expression of suppressor of cytokine signaling 3, vascular cell adhesion molecule 1, reactive oxygen species, nitrotyrosine, and endothelin-1 in the periodontitis group was more intense than that in the control group. Significantly decreased levels of phosphatidylinositol 3-kinase (Pi3k) catalytic β-polypeptide (Pi3kcb), Pi3kp85, and insulin receptor substrate 1 and 2 were observed in the periodontitis group. Levels of serum CRP and TNF-α were significantly increased in the periodontitis group. Under insulin-stimulated conditions, aorta in the periodontitis group altered the Akt phosphorylation. Periodontitis in obesity induced the initial stage of atherosclerosis and disturbed aortic insulin signaling. |
doi_str_mv | 10.1038/labinvest.2009.141 |
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However, the effects of periodontitis on atherosclerosis in an obese body remain unclear. The aim of the study was to investigate the effects of ligature-induced periodontitis in Zucker fatty rats on initiation of atherosclerosis by evaluating aortic insulin resistance. Zucker fatty rats (n=24) were divided into two groups. In the periodontitis group, periodontitis was ligature-induced for 4 weeks, whereas the control group was left unligated. After the 4-week experimental period, descending aorta was used for measuring the levels of lipid deposits, immunohistochemical analysis, and evaluation of gene expression. Levels of serum C-reactive protein (CRP), tumor necrosis factor-α (TNF-α), and insulin were also measured. Rats in the periodontitis group had significantly enhanced lipid deposits in the aorta, but not in the control group. Expression of suppressor of cytokine signaling 3, vascular cell adhesion molecule 1, reactive oxygen species, nitrotyrosine, and endothelin-1 in the periodontitis group was more intense than that in the control group. Significantly decreased levels of phosphatidylinositol 3-kinase (Pi3k) catalytic β-polypeptide (Pi3kcb), Pi3kp85, and insulin receptor substrate 1 and 2 were observed in the periodontitis group. Levels of serum CRP and TNF-α were significantly increased in the periodontitis group. Under insulin-stimulated conditions, aorta in the periodontitis group altered the Akt phosphorylation. Periodontitis in obesity induced the initial stage of atherosclerosis and disturbed aortic insulin signaling.</description><identifier>ISSN: 0023-6837</identifier><identifier>EISSN: 1530-0307</identifier><identifier>DOI: 10.1038/labinvest.2009.141</identifier><identifier>PMID: 20065945</identifier><identifier>CODEN: LAINAW</identifier><language>eng</language><publisher>New York: Elsevier Inc</publisher><subject>692/699/249/2510 ; 692/699/2743/393 ; 692/699/317 ; 692/699/75/593/2100 ; animal models ; Animals ; Aorta - metabolism ; atherosclerosis ; Atherosclerosis - etiology ; Atherosclerosis - metabolism ; Biological and medical sciences ; Biotechnology ; Endothelin-1 - metabolism ; Facial bones, jaws, teeth, parodontium: diseases, semeiology ; Fundamental and applied biological sciences. Psychology ; Gene Expression Profiling ; Insulin Resistance ; Investigative techniques, diagnostic techniques (general aspects) ; Laboratory Medicine ; Ligation ; Male ; Medical sciences ; Medicine ; Medicine & Public Health ; Non tumoral diseases ; obesity ; Obesity - complications ; Obesity - metabolism ; Oligonucleotide Array Sequence Analysis ; Otorhinolaryngology. Stomatology ; Pathology ; periodontal disease ; Periodontitis - complications ; Periodontitis - metabolism ; Phosphatidylinositol 3-Kinases - metabolism ; Proto-Oncogene Proteins c-akt - metabolism ; Rats ; Rats, Zucker ; research-article ; Vascular Cell Adhesion Molecule-1 - metabolism ; Vascular Endothelial Growth Factor A - metabolism</subject><ispartof>Laboratory investigation, 2010-03, Vol.90 (3), p.348-359</ispartof><rights>2010 United States & Canadian Academy of Pathology</rights><rights>United States and Canadian Academy of Pathology, Inc. 2010</rights><rights>2015 INIST-CNRS</rights><rights>Copyright Nature Publishing Group Mar 2010</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c566t-a6940a1c77206d1f09068f189cd2b346e0194f1adf0789d15e2ab6014bda943d3</citedby><cites>FETCH-LOGICAL-c566t-a6940a1c77206d1f09068f189cd2b346e0194f1adf0789d15e2ab6014bda943d3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=22546095$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/20065945$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ekuni, Daisuke</creatorcontrib><creatorcontrib>Tomofuji, Takaaki</creatorcontrib><creatorcontrib>Irie, Koichiro</creatorcontrib><creatorcontrib>Kasuyama, Kenta</creatorcontrib><creatorcontrib>Umakoshi, Michihiro</creatorcontrib><creatorcontrib>Azuma, Tetsuji</creatorcontrib><creatorcontrib>Tamaki, Naofumi</creatorcontrib><creatorcontrib>Sanbe, Toshihiro</creatorcontrib><creatorcontrib>Endo, Yasumasa</creatorcontrib><creatorcontrib>Yamamoto, Tatsuo</creatorcontrib><creatorcontrib>Nishida, Takashi</creatorcontrib><creatorcontrib>Morita, Manabu</creatorcontrib><title>Effects of periodontitis on aortic insulin resistance in an obese rat model</title><title>Laboratory investigation</title><addtitle>Lab Invest</addtitle><addtitle>Lab Invest</addtitle><description>The combination of obesity and its associated risk factors, such as insulin resistance and inflammation, results in the development of atherosclerosis. However, the effects of periodontitis on atherosclerosis in an obese body remain unclear. The aim of the study was to investigate the effects of ligature-induced periodontitis in Zucker fatty rats on initiation of atherosclerosis by evaluating aortic insulin resistance. Zucker fatty rats (n=24) were divided into two groups. In the periodontitis group, periodontitis was ligature-induced for 4 weeks, whereas the control group was left unligated. After the 4-week experimental period, descending aorta was used for measuring the levels of lipid deposits, immunohistochemical analysis, and evaluation of gene expression. Levels of serum C-reactive protein (CRP), tumor necrosis factor-α (TNF-α), and insulin were also measured. Rats in the periodontitis group had significantly enhanced lipid deposits in the aorta, but not in the control group. Expression of suppressor of cytokine signaling 3, vascular cell adhesion molecule 1, reactive oxygen species, nitrotyrosine, and endothelin-1 in the periodontitis group was more intense than that in the control group. Significantly decreased levels of phosphatidylinositol 3-kinase (Pi3k) catalytic β-polypeptide (Pi3kcb), Pi3kp85, and insulin receptor substrate 1 and 2 were observed in the periodontitis group. Levels of serum CRP and TNF-α were significantly increased in the periodontitis group. Under insulin-stimulated conditions, aorta in the periodontitis group altered the Akt phosphorylation. Periodontitis in obesity induced the initial stage of atherosclerosis and disturbed aortic insulin signaling.</description><subject>692/699/249/2510</subject><subject>692/699/2743/393</subject><subject>692/699/317</subject><subject>692/699/75/593/2100</subject><subject>animal models</subject><subject>Animals</subject><subject>Aorta - metabolism</subject><subject>atherosclerosis</subject><subject>Atherosclerosis - etiology</subject><subject>Atherosclerosis - metabolism</subject><subject>Biological and medical sciences</subject><subject>Biotechnology</subject><subject>Endothelin-1 - metabolism</subject><subject>Facial bones, jaws, teeth, parodontium: diseases, semeiology</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Gene Expression Profiling</subject><subject>Insulin Resistance</subject><subject>Investigative techniques, diagnostic techniques (general aspects)</subject><subject>Laboratory Medicine</subject><subject>Ligation</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Non tumoral diseases</subject><subject>obesity</subject><subject>Obesity - complications</subject><subject>Obesity - metabolism</subject><subject>Oligonucleotide Array Sequence Analysis</subject><subject>Otorhinolaryngology. Stomatology</subject><subject>Pathology</subject><subject>periodontal disease</subject><subject>Periodontitis - complications</subject><subject>Periodontitis - metabolism</subject><subject>Phosphatidylinositol 3-Kinases - metabolism</subject><subject>Proto-Oncogene Proteins c-akt - metabolism</subject><subject>Rats</subject><subject>Rats, Zucker</subject><subject>research-article</subject><subject>Vascular Cell Adhesion Molecule-1 - metabolism</subject><subject>Vascular Endothelial Growth Factor A - metabolism</subject><issn>0023-6837</issn><issn>1530-0307</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNp9kU1rVDEUhoModlr9Ay4kCOLqjiefNwE3pdQqFtzoOuTmQ1LuJGNyb8F_b4YZW3DRVeDkeU9OnoPQGwJbAkx9nO2U8n1oy5YC6C3h5BnaEMFgAAbjc7QBoGyQio1n6Ly1OwDCuRQv0VnnpdBcbNC36xiDWxouEe9DTcWXvKQl9ULGttQlOZxyW-eUcQ0ttcVmF3oJ24zLFFrA1S54V3yYX6EX0c4tvD6dF-jn5-sfV1-G2-83X68ubwcnpFwGKzUHS9w4UpCeRNAgVSRKO08nxmUAonkk1kcYlfZEBGon2WefvNWceXaBPhz77mv5vfb_m11qLsyzzaGszYyMCQUjIZ189x95V9aa-3CGUqBKaKU6RI-Qq6W1GqLZ17Sz9Y8hYA6izYNocxBtuugeenvqvE674B8i_8x24P0JsM3ZOdbuLbVHjgouQR84duRav8q_Qn0c8cnnPx1ToXu-Tz3VXAp9Mz7Vvk7jS3oq_hdgT63s</recordid><startdate>20100301</startdate><enddate>20100301</enddate><creator>Ekuni, Daisuke</creator><creator>Tomofuji, Takaaki</creator><creator>Irie, Koichiro</creator><creator>Kasuyama, Kenta</creator><creator>Umakoshi, Michihiro</creator><creator>Azuma, Tetsuji</creator><creator>Tamaki, Naofumi</creator><creator>Sanbe, Toshihiro</creator><creator>Endo, Yasumasa</creator><creator>Yamamoto, Tatsuo</creator><creator>Nishida, Takashi</creator><creator>Morita, Manabu</creator><general>Elsevier Inc</general><general>Nature Publishing Group US</general><general>Nature Publishing Group</general><scope>6I.</scope><scope>AAFTH</scope><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>3V.</scope><scope>7QL</scope><scope>7QP</scope><scope>7QR</scope><scope>7T5</scope><scope>7T7</scope><scope>7TK</scope><scope>7TM</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</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>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</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>M7N</scope><scope>M7P</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>7X8</scope></search><sort><creationdate>20100301</creationdate><title>Effects of periodontitis on aortic insulin resistance in an obese rat model</title><author>Ekuni, Daisuke ; Tomofuji, Takaaki ; Irie, Koichiro ; Kasuyama, Kenta ; Umakoshi, Michihiro ; Azuma, Tetsuji ; Tamaki, Naofumi ; Sanbe, Toshihiro ; Endo, Yasumasa ; Yamamoto, Tatsuo ; Nishida, Takashi ; Morita, Manabu</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c566t-a6940a1c77206d1f09068f189cd2b346e0194f1adf0789d15e2ab6014bda943d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2010</creationdate><topic>692/699/249/2510</topic><topic>692/699/2743/393</topic><topic>692/699/317</topic><topic>692/699/75/593/2100</topic><topic>animal models</topic><topic>Animals</topic><topic>Aorta - metabolism</topic><topic>atherosclerosis</topic><topic>Atherosclerosis - etiology</topic><topic>Atherosclerosis - metabolism</topic><topic>Biological and medical sciences</topic><topic>Biotechnology</topic><topic>Endothelin-1 - metabolism</topic><topic>Facial bones, jaws, teeth, parodontium: diseases, semeiology</topic><topic>Fundamental and applied biological sciences. 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However, the effects of periodontitis on atherosclerosis in an obese body remain unclear. The aim of the study was to investigate the effects of ligature-induced periodontitis in Zucker fatty rats on initiation of atherosclerosis by evaluating aortic insulin resistance. Zucker fatty rats (n=24) were divided into two groups. In the periodontitis group, periodontitis was ligature-induced for 4 weeks, whereas the control group was left unligated. After the 4-week experimental period, descending aorta was used for measuring the levels of lipid deposits, immunohistochemical analysis, and evaluation of gene expression. Levels of serum C-reactive protein (CRP), tumor necrosis factor-α (TNF-α), and insulin were also measured. Rats in the periodontitis group had significantly enhanced lipid deposits in the aorta, but not in the control group. Expression of suppressor of cytokine signaling 3, vascular cell adhesion molecule 1, reactive oxygen species, nitrotyrosine, and endothelin-1 in the periodontitis group was more intense than that in the control group. Significantly decreased levels of phosphatidylinositol 3-kinase (Pi3k) catalytic β-polypeptide (Pi3kcb), Pi3kp85, and insulin receptor substrate 1 and 2 were observed in the periodontitis group. Levels of serum CRP and TNF-α were significantly increased in the periodontitis group. Under insulin-stimulated conditions, aorta in the periodontitis group altered the Akt phosphorylation. Periodontitis in obesity induced the initial stage of atherosclerosis and disturbed aortic insulin signaling.</abstract><cop>New York</cop><pub>Elsevier Inc</pub><pmid>20065945</pmid><doi>10.1038/labinvest.2009.141</doi><tpages>12</tpages><oa>free_for_read</oa></addata></record> |
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subjects | 692/699/249/2510 692/699/2743/393 692/699/317 692/699/75/593/2100 animal models Animals Aorta - metabolism atherosclerosis Atherosclerosis - etiology Atherosclerosis - metabolism Biological and medical sciences Biotechnology Endothelin-1 - metabolism Facial bones, jaws, teeth, parodontium: diseases, semeiology Fundamental and applied biological sciences. Psychology Gene Expression Profiling Insulin Resistance Investigative techniques, diagnostic techniques (general aspects) Laboratory Medicine Ligation Male Medical sciences Medicine Medicine & Public Health Non tumoral diseases obesity Obesity - complications Obesity - metabolism Oligonucleotide Array Sequence Analysis Otorhinolaryngology. Stomatology Pathology periodontal disease Periodontitis - complications Periodontitis - metabolism Phosphatidylinositol 3-Kinases - metabolism Proto-Oncogene Proteins c-akt - metabolism Rats Rats, Zucker research-article Vascular Cell Adhesion Molecule-1 - metabolism Vascular Endothelial Growth Factor A - metabolism |
title | Effects of periodontitis on aortic insulin resistance in an obese rat model |
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