Gene expression profiling supports the role of Repin1 in the pathophysiology of metabolic syndrome
Congenic BB rat strains carrying a SHR segment (D4Got41-Tacr1; 60.5–122.8 Mb; BB.4S) or a WOKW segment (D4Got41-Fabp1; 60.5–104.6 Mb; BB.4W) of chromosome 4 within the BB/OK background develop facets of the metabolic syndrome when compared with their parental BB/OK rats. To narrow down potential gen...
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Veröffentlicht in: | Endocrine 2011-10, Vol.40 (2), p.310-314 |
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description | Congenic BB rat strains carrying a SHR segment (D4Got41-Tacr1; 60.5–122.8 Mb; BB.4S) or a WOKW segment (D4Got41-Fabp1; 60.5–104.6 Mb; BB.4W) of chromosome 4 within the BB/OK background develop facets of the metabolic syndrome when compared with their parental BB/OK rats. To narrow down potential genes involved in the pathophysiology of metabolic syndrome, gene expression studies in adipose tissues of BB/OK, BB.4S, and BB.4W rats were initiated. Total RNA of subcutaneous and epididymal adipose tissue of BB/OK (
n
= 10), congenic BB.4S (
n
= 8), and BB.4W (
n
= 9) males at an age of 4 weeks was isolated. The mRNA expression of 92 genes involved in obesity, insulin resistance and other metabolic traits was measured by RT-PCR. Significant differences in gene expression were only found in
Repin1
in both adipose tissues. Congenic BB.4W showed significantly lower gene expression than did BB.4S and BB/OK. Our findings and newly published findings of
Repin1
in 3T3-L1 adipocytes support the hypothesis that
Repin1
may affect the development of facets of the metabolic syndrome. |
doi_str_mv | 10.1007/s12020-011-9497-7 |
format | Article |
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n
= 10), congenic BB.4S (
n
= 8), and BB.4W (
n
= 9) males at an age of 4 weeks was isolated. The mRNA expression of 92 genes involved in obesity, insulin resistance and other metabolic traits was measured by RT-PCR. Significant differences in gene expression were only found in
Repin1
in both adipose tissues. Congenic BB.4W showed significantly lower gene expression than did BB.4S and BB/OK. Our findings and newly published findings of
Repin1
in 3T3-L1 adipocytes support the hypothesis that
Repin1
may affect the development of facets of the metabolic syndrome.</description><identifier>ISSN: 1355-008X</identifier><identifier>EISSN: 1559-0100</identifier><identifier>DOI: 10.1007/s12020-011-9497-7</identifier><identifier>PMID: 21701954</identifier><language>eng</language><publisher>Boston: Springer US</publisher><subject>Adipose Tissue, White - metabolism ; Animals ; Animals, Congenic ; Diabetes ; Disease Models, Animal ; DNA-Binding Proteins - genetics ; DNA-Binding Proteins - metabolism ; Endocrinology ; Epididymis ; Fatty Acid-Binding Proteins - genetics ; Gene Expression Profiling ; Humanities and Social Sciences ; Internal Medicine ; Male ; Medicine ; Medicine & Public Health ; Metabolic Syndrome - metabolism ; multidisciplinary ; Rats ; Rats, Inbred BB ; Receptors, Neurokinin-1 - genetics ; Research Letter ; RNA, Messenger - metabolism ; Science ; Specific Pathogen-Free Organisms ; Subcutaneous Fat - metabolism ; Up-Regulation</subject><ispartof>Endocrine, 2011-10, Vol.40 (2), p.310-314</ispartof><rights>Springer Science+Business Media, LLC 2011</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c343t-f45d7f001c0f80cf6f54fca156955a571dc4ce1a0e6970a10ca8c6f650000c693</citedby><cites>FETCH-LOGICAL-c343t-f45d7f001c0f80cf6f54fca156955a571dc4ce1a0e6970a10ca8c6f650000c693</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s12020-011-9497-7$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s12020-011-9497-7$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,780,784,27922,27923,41486,42555,51317</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/21701954$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Bahr, Jeanette</creatorcontrib><creatorcontrib>Klöting, Nora</creatorcontrib><creatorcontrib>Klöting, Ingrid</creatorcontrib><creatorcontrib>Follak, Niels</creatorcontrib><title>Gene expression profiling supports the role of Repin1 in the pathophysiology of metabolic syndrome</title><title>Endocrine</title><addtitle>Endocrine</addtitle><addtitle>Endocrine</addtitle><description>Congenic BB rat strains carrying a SHR segment (D4Got41-Tacr1; 60.5–122.8 Mb; BB.4S) or a WOKW segment (D4Got41-Fabp1; 60.5–104.6 Mb; BB.4W) of chromosome 4 within the BB/OK background develop facets of the metabolic syndrome when compared with their parental BB/OK rats. To narrow down potential genes involved in the pathophysiology of metabolic syndrome, gene expression studies in adipose tissues of BB/OK, BB.4S, and BB.4W rats were initiated. Total RNA of subcutaneous and epididymal adipose tissue of BB/OK (
n
= 10), congenic BB.4S (
n
= 8), and BB.4W (
n
= 9) males at an age of 4 weeks was isolated. The mRNA expression of 92 genes involved in obesity, insulin resistance and other metabolic traits was measured by RT-PCR. Significant differences in gene expression were only found in
Repin1
in both adipose tissues. Congenic BB.4W showed significantly lower gene expression than did BB.4S and BB/OK. Our findings and newly published findings of
Repin1
in 3T3-L1 adipocytes support the hypothesis that
Repin1
may affect the development of facets of the metabolic syndrome.</description><subject>Adipose Tissue, White - metabolism</subject><subject>Animals</subject><subject>Animals, Congenic</subject><subject>Diabetes</subject><subject>Disease Models, Animal</subject><subject>DNA-Binding Proteins - genetics</subject><subject>DNA-Binding Proteins - metabolism</subject><subject>Endocrinology</subject><subject>Epididymis</subject><subject>Fatty Acid-Binding Proteins - genetics</subject><subject>Gene Expression Profiling</subject><subject>Humanities and Social Sciences</subject><subject>Internal Medicine</subject><subject>Male</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Metabolic Syndrome - metabolism</subject><subject>multidisciplinary</subject><subject>Rats</subject><subject>Rats, Inbred BB</subject><subject>Receptors, Neurokinin-1 - genetics</subject><subject>Research Letter</subject><subject>RNA, Messenger - metabolism</subject><subject>Science</subject><subject>Specific Pathogen-Free Organisms</subject><subject>Subcutaneous Fat - metabolism</subject><subject>Up-Regulation</subject><issn>1355-008X</issn><issn>1559-0100</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kEFLwzAYhoMobk5_gBfJzVP1S9c0zVGGTkEQRMFbyLIvW0eb1KQF9-_N3PRoLglfnveF7yHkksENAxC3keWQQwaMZbKQIhNHZMw4l2kCcJzeU84zgOpjRM5i3ADkeV6KUzLKmQAmeTEmizk6pPjVBYyx9o52wdu6qd2KxqHrfOgj7ddIg2-Qektfsasdo7X7mXa6X_tuvU3Jxq-2O6DFXi98Uxsat24ZfIvn5MTqJuLF4Z6Q94f7t9lj9vwyf5rdPWdmWkz7zBZ8KSwAM2ArMLa0vLBGM15KzjUXbGkKg0wDllKAZmB0ZUpbckjHlHI6Idf73rTC54CxV20dDTaNduiHqCrJKy65hESyPWmCjzGgVV2oWx22ioHamVV7syqZVTuzSqTM1aF9WLS4_Ev8qkxAvgdi-nIrDGrjh-DSxv-0fgP7lYUL</recordid><startdate>20111001</startdate><enddate>20111001</enddate><creator>Bahr, Jeanette</creator><creator>Klöting, Nora</creator><creator>Klöting, Ingrid</creator><creator>Follak, Niels</creator><general>Springer US</general><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>7X8</scope></search><sort><creationdate>20111001</creationdate><title>Gene expression profiling supports the role of Repin1 in the pathophysiology of metabolic syndrome</title><author>Bahr, Jeanette ; Klöting, Nora ; Klöting, Ingrid ; Follak, Niels</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c343t-f45d7f001c0f80cf6f54fca156955a571dc4ce1a0e6970a10ca8c6f650000c693</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2011</creationdate><topic>Adipose Tissue, White - metabolism</topic><topic>Animals</topic><topic>Animals, Congenic</topic><topic>Diabetes</topic><topic>Disease Models, Animal</topic><topic>DNA-Binding Proteins - genetics</topic><topic>DNA-Binding Proteins - metabolism</topic><topic>Endocrinology</topic><topic>Epididymis</topic><topic>Fatty Acid-Binding Proteins - genetics</topic><topic>Gene Expression Profiling</topic><topic>Humanities and Social Sciences</topic><topic>Internal Medicine</topic><topic>Male</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Metabolic Syndrome - metabolism</topic><topic>multidisciplinary</topic><topic>Rats</topic><topic>Rats, Inbred BB</topic><topic>Receptors, Neurokinin-1 - genetics</topic><topic>Research Letter</topic><topic>RNA, Messenger - metabolism</topic><topic>Science</topic><topic>Specific Pathogen-Free Organisms</topic><topic>Subcutaneous Fat - metabolism</topic><topic>Up-Regulation</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Bahr, Jeanette</creatorcontrib><creatorcontrib>Klöting, Nora</creatorcontrib><creatorcontrib>Klöting, Ingrid</creatorcontrib><creatorcontrib>Follak, Niels</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Endocrine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Bahr, Jeanette</au><au>Klöting, Nora</au><au>Klöting, Ingrid</au><au>Follak, Niels</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Gene expression profiling supports the role of Repin1 in the pathophysiology of metabolic syndrome</atitle><jtitle>Endocrine</jtitle><stitle>Endocrine</stitle><addtitle>Endocrine</addtitle><date>2011-10-01</date><risdate>2011</risdate><volume>40</volume><issue>2</issue><spage>310</spage><epage>314</epage><pages>310-314</pages><issn>1355-008X</issn><eissn>1559-0100</eissn><abstract>Congenic BB rat strains carrying a SHR segment (D4Got41-Tacr1; 60.5–122.8 Mb; BB.4S) or a WOKW segment (D4Got41-Fabp1; 60.5–104.6 Mb; BB.4W) of chromosome 4 within the BB/OK background develop facets of the metabolic syndrome when compared with their parental BB/OK rats. To narrow down potential genes involved in the pathophysiology of metabolic syndrome, gene expression studies in adipose tissues of BB/OK, BB.4S, and BB.4W rats were initiated. Total RNA of subcutaneous and epididymal adipose tissue of BB/OK (
n
= 10), congenic BB.4S (
n
= 8), and BB.4W (
n
= 9) males at an age of 4 weeks was isolated. The mRNA expression of 92 genes involved in obesity, insulin resistance and other metabolic traits was measured by RT-PCR. Significant differences in gene expression were only found in
Repin1
in both adipose tissues. Congenic BB.4W showed significantly lower gene expression than did BB.4S and BB/OK. Our findings and newly published findings of
Repin1
in 3T3-L1 adipocytes support the hypothesis that
Repin1
may affect the development of facets of the metabolic syndrome.</abstract><cop>Boston</cop><pub>Springer US</pub><pmid>21701954</pmid><doi>10.1007/s12020-011-9497-7</doi><tpages>5</tpages></addata></record> |
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subjects | Adipose Tissue, White - metabolism Animals Animals, Congenic Diabetes Disease Models, Animal DNA-Binding Proteins - genetics DNA-Binding Proteins - metabolism Endocrinology Epididymis Fatty Acid-Binding Proteins - genetics Gene Expression Profiling Humanities and Social Sciences Internal Medicine Male Medicine Medicine & Public Health Metabolic Syndrome - metabolism multidisciplinary Rats Rats, Inbred BB Receptors, Neurokinin-1 - genetics Research Letter RNA, Messenger - metabolism Science Specific Pathogen-Free Organisms Subcutaneous Fat - metabolism Up-Regulation |
title | Gene expression profiling supports the role of Repin1 in the pathophysiology of metabolic syndrome |
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