Decreased Thioredoxin-1 and Increased HSP90 Expression in Skeletal Muscle in Subjects with Type 2 Diabetes or Impaired Glucose Tolerance
In diabetes, the endogenous defence systems are overwhelmed, causing various types of stress in tissues. In this study, newly diagnosed or diet-treated type 2 diabetics (T2D) (n=10) were compared with subjects with impaired glucose tolerance (IGT) (n=8). In both groups, at resting conditions, blood...
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| Veröffentlicht in: | BioMed research international 2014-01, Vol.2014 (2014), p.1-6 |
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| creator | Venojärvi, M. Korkmaz, A. Aunola, S. Hällsten, K. Virtanen, K. Marniemi, J. Halonen, J.-P. Hänninen, O. Nuutila, P. Atalay, M. |
| description | In diabetes, the endogenous defence systems are overwhelmed, causing various types of stress in tissues. In this study, newly diagnosed or diet-treated type 2 diabetics (T2D) (n=10) were compared with subjects with impaired glucose tolerance (IGT) (n=8). In both groups, at resting conditions, blood samples were drawn for assessing metabolic indices and skeletal muscle samples (m. vastus lateralis) were taken for the measurements of cellular defence markers: thioredoxin-1 (TRX-1) and stress proteins HSP72, HSP90. The protein level of TRX-1 was 36.1% lower (P=0.031) and HSP90 was 380% higher (P |
| doi_str_mv | 10.1155/2014/386351 |
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In this study, newly diagnosed or diet-treated type 2 diabetics (T2D) (n=10) were compared with subjects with impaired glucose tolerance (IGT) (n=8). In both groups, at resting conditions, blood samples were drawn for assessing metabolic indices and skeletal muscle samples (m. vastus lateralis) were taken for the measurements of cellular defence markers: thioredoxin-1 (TRX-1) and stress proteins HSP72, HSP90. The protein level of TRX-1 was 36.1% lower (P=0.031) and HSP90 was 380% higher (P<0.001) in the T2D than in the IGT subjects, with no significant changes in HSP72. However, after the adjustment of both analyses with HOMA-IR only HSP90 difference remained significant. In conclusion, level of TRX-1 in skeletal muscle tissue was lower while that of HSP90 was higher in T2D than in IGT subjects. This may impair antioxidant defence and lead to disruptions of protein homoeostasis and redox regulation of cellular defences. Because HSP90 may be involved in sustaining functional insulin signalling pathway in type 2 diabetic muscles and higher HSP90 levels can be a consequence of type 2 diabetes, our results are potentially important for the diabetes research.</description><identifier>ISSN: 2314-6133</identifier><identifier>EISSN: 2314-6141</identifier><identifier>DOI: 10.1155/2014/386351</identifier><identifier>PMID: 24689038</identifier><language>eng</language><publisher>Cairo, Egypt: Hindawi Puplishing Corporation</publisher><subject>Biomedical research ; Blood Glucose - metabolism ; Diabetes Mellitus, Type 2 - metabolism ; Diabetes Mellitus, Type 2 - pathology ; Female ; Glucose ; Glucose intolerance ; Glucose Intolerance - metabolism ; Glucose Intolerance - pathology ; Health aspects ; Heat shock proteins ; HSP72 Heat-Shock Proteins - metabolism ; HSP90 Heat-Shock Proteins - metabolism ; Humans ; Insulin ; Kinases ; Male ; Middle Aged ; Muscle, Skeletal - metabolism ; Muscle, Skeletal - pathology ; Muscles ; Muscular system ; Physiological aspects ; Rodents ; Thioredoxin ; Thioredoxins - metabolism ; Type 2 diabetes</subject><ispartof>BioMed research international, 2014-01, Vol.2014 (2014), p.1-6</ispartof><rights>Copyright © 2014 M. Venojärvi et al.</rights><rights>COPYRIGHT 2014 John Wiley & Sons, Inc.</rights><rights>Copyright © 2014 M. Venojärvi et al. M. Venojärvi et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.</rights><rights>Copyright © 2014 M. Venojärvi et al. 2014</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c527t-a37433e8c2864716db7447ec081d09333308e48b5d53b5c91843ec1da16ba23c3</citedby><cites>FETCH-LOGICAL-c527t-a37433e8c2864716db7447ec081d09333308e48b5d53b5c91843ec1da16ba23c3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3932292/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3932292/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24689038$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Kushnir, Mark M.</contributor><creatorcontrib>Venojärvi, M.</creatorcontrib><creatorcontrib>Korkmaz, A.</creatorcontrib><creatorcontrib>Aunola, S.</creatorcontrib><creatorcontrib>Hällsten, K.</creatorcontrib><creatorcontrib>Virtanen, K.</creatorcontrib><creatorcontrib>Marniemi, J.</creatorcontrib><creatorcontrib>Halonen, J.-P.</creatorcontrib><creatorcontrib>Hänninen, O.</creatorcontrib><creatorcontrib>Nuutila, P.</creatorcontrib><creatorcontrib>Atalay, M.</creatorcontrib><title>Decreased Thioredoxin-1 and Increased HSP90 Expression in Skeletal Muscle in Subjects with Type 2 Diabetes or Impaired Glucose Tolerance</title><title>BioMed research international</title><addtitle>Biomed Res Int</addtitle><description>In diabetes, the endogenous defence systems are overwhelmed, causing various types of stress in tissues. In this study, newly diagnosed or diet-treated type 2 diabetics (T2D) (n=10) were compared with subjects with impaired glucose tolerance (IGT) (n=8). In both groups, at resting conditions, blood samples were drawn for assessing metabolic indices and skeletal muscle samples (m. vastus lateralis) were taken for the measurements of cellular defence markers: thioredoxin-1 (TRX-1) and stress proteins HSP72, HSP90. The protein level of TRX-1 was 36.1% lower (P=0.031) and HSP90 was 380% higher (P<0.001) in the T2D than in the IGT subjects, with no significant changes in HSP72. However, after the adjustment of both analyses with HOMA-IR only HSP90 difference remained significant. In conclusion, level of TRX-1 in skeletal muscle tissue was lower while that of HSP90 was higher in T2D than in IGT subjects. This may impair antioxidant defence and lead to disruptions of protein homoeostasis and redox regulation of cellular defences. Because HSP90 may be involved in sustaining functional insulin signalling pathway in type 2 diabetic muscles and higher HSP90 levels can be a consequence of type 2 diabetes, our results are potentially important for the diabetes research.</description><subject>Biomedical research</subject><subject>Blood Glucose - metabolism</subject><subject>Diabetes Mellitus, Type 2 - metabolism</subject><subject>Diabetes Mellitus, Type 2 - pathology</subject><subject>Female</subject><subject>Glucose</subject><subject>Glucose intolerance</subject><subject>Glucose Intolerance - metabolism</subject><subject>Glucose Intolerance - pathology</subject><subject>Health aspects</subject><subject>Heat shock proteins</subject><subject>HSP72 Heat-Shock Proteins - metabolism</subject><subject>HSP90 Heat-Shock Proteins - metabolism</subject><subject>Humans</subject><subject>Insulin</subject><subject>Kinases</subject><subject>Male</subject><subject>Middle Aged</subject><subject>Muscle, Skeletal - metabolism</subject><subject>Muscle, Skeletal - pathology</subject><subject>Muscles</subject><subject>Muscular system</subject><subject>Physiological aspects</subject><subject>Rodents</subject><subject>Thioredoxin</subject><subject>Thioredoxins - metabolism</subject><subject>Type 2 diabetes</subject><issn>2314-6133</issn><issn>2314-6141</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>RHX</sourceid><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNqNkktv1DAURiMEolXpijXIEhsECvUrjrNBqtrSjlQEUoe15Th3Oh48dmontP0H_dn1kHZ4bMAbW75Hx75XX1G8JPgDIVV1QDHhB0wKVpEnxS5lhJeCcPJ0e2Zsp9hPaYXzkkTgRjwvdigXssFM7hZ3x2Ai6AQdmi9tiNCFG-tLgrTv0Mw_1s4uvjYYndz0EVKywSPr0cV3cDBohz6PyTj4eTW2KzBDQtd2WKL5bQ-IomOrWxggoRDRbN1rmx9Bp240IQGaBwdRewMvimcL7RLsP-x7xbdPJ_Ojs_L8y-ns6PC8NBWth1KzmjMG0lApeE1E19ac12Bybx1uWF5YApdt1VWsrUxDJGdgSKeJaDVlhu0VHydvP7Zr6Az4IWqn-mjXOt6qoK36s-LtUl2GH4o1jNKGZsHbB0EMVyOkQa1tMuCc9hDGpEjFuKQUM_IfKKGUCoZxRt_8ha7CGH2eRKZwNsqs_UVdagfK-kXIXzQbqTrktMaUymrjej9RJoaUIiy23RGsNqlRm9SoKTWZfv37QLbsY0Yy8G4CltZ3-tr-w_ZqgiEjsNBbONswEeweFuvQXg</recordid><startdate>20140101</startdate><enddate>20140101</enddate><creator>Venojärvi, M.</creator><creator>Korkmaz, A.</creator><creator>Aunola, S.</creator><creator>Hällsten, K.</creator><creator>Virtanen, K.</creator><creator>Marniemi, J.</creator><creator>Halonen, J.-P.</creator><creator>Hänninen, O.</creator><creator>Nuutila, P.</creator><creator>Atalay, M.</creator><general>Hindawi Puplishing Corporation</general><general>Hindawi Publishing Corporation</general><general>John Wiley & Sons, Inc</general><general>Hindawi Limited</general><scope>ADJCN</scope><scope>AHFXO</scope><scope>RHU</scope><scope>RHW</scope><scope>RHX</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>7QO</scope><scope>7T7</scope><scope>7TK</scope><scope>7U7</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>CWDGH</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>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20140101</creationdate><title>Decreased Thioredoxin-1 and Increased HSP90 Expression in Skeletal Muscle in Subjects with Type 2 Diabetes or Impaired Glucose Tolerance</title><author>Venojärvi, M. ; Korkmaz, A. ; Aunola, S. ; Hällsten, K. ; Virtanen, K. ; Marniemi, J. ; Halonen, J.-P. ; Hänninen, O. ; Nuutila, P. ; Atalay, M.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c527t-a37433e8c2864716db7447ec081d09333308e48b5d53b5c91843ec1da16ba23c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>Biomedical research</topic><topic>Blood Glucose - metabolism</topic><topic>Diabetes Mellitus, Type 2 - metabolism</topic><topic>Diabetes Mellitus, Type 2 - pathology</topic><topic>Female</topic><topic>Glucose</topic><topic>Glucose intolerance</topic><topic>Glucose Intolerance - metabolism</topic><topic>Glucose Intolerance - pathology</topic><topic>Health aspects</topic><topic>Heat shock proteins</topic><topic>HSP72 Heat-Shock Proteins - metabolism</topic><topic>HSP90 Heat-Shock Proteins - metabolism</topic><topic>Humans</topic><topic>Insulin</topic><topic>Kinases</topic><topic>Male</topic><topic>Middle Aged</topic><topic>Muscle, Skeletal - metabolism</topic><topic>Muscle, Skeletal - pathology</topic><topic>Muscles</topic><topic>Muscular system</topic><topic>Physiological aspects</topic><topic>Rodents</topic><topic>Thioredoxin</topic><topic>Thioredoxins - metabolism</topic><topic>Type 2 diabetes</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Venojärvi, M.</creatorcontrib><creatorcontrib>Korkmaz, A.</creatorcontrib><creatorcontrib>Aunola, S.</creatorcontrib><creatorcontrib>Hällsten, K.</creatorcontrib><creatorcontrib>Virtanen, K.</creatorcontrib><creatorcontrib>Marniemi, J.</creatorcontrib><creatorcontrib>Halonen, J.-P.</creatorcontrib><creatorcontrib>Hänninen, O.</creatorcontrib><creatorcontrib>Nuutila, P.</creatorcontrib><creatorcontrib>Atalay, M.</creatorcontrib><collection>الدوريات العلمية والإحصائية - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>BioMed research international</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Venojärvi, M.</au><au>Korkmaz, A.</au><au>Aunola, S.</au><au>Hällsten, K.</au><au>Virtanen, K.</au><au>Marniemi, J.</au><au>Halonen, J.-P.</au><au>Hänninen, O.</au><au>Nuutila, P.</au><au>Atalay, M.</au><au>Kushnir, Mark M.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Decreased Thioredoxin-1 and Increased HSP90 Expression in Skeletal Muscle in Subjects with Type 2 Diabetes or Impaired Glucose Tolerance</atitle><jtitle>BioMed research international</jtitle><addtitle>Biomed Res Int</addtitle><date>2014-01-01</date><risdate>2014</risdate><volume>2014</volume><issue>2014</issue><spage>1</spage><epage>6</epage><pages>1-6</pages><issn>2314-6133</issn><eissn>2314-6141</eissn><abstract>In diabetes, the endogenous defence systems are overwhelmed, causing various types of stress in tissues. In this study, newly diagnosed or diet-treated type 2 diabetics (T2D) (n=10) were compared with subjects with impaired glucose tolerance (IGT) (n=8). In both groups, at resting conditions, blood samples were drawn for assessing metabolic indices and skeletal muscle samples (m. vastus lateralis) were taken for the measurements of cellular defence markers: thioredoxin-1 (TRX-1) and stress proteins HSP72, HSP90. The protein level of TRX-1 was 36.1% lower (P=0.031) and HSP90 was 380% higher (P<0.001) in the T2D than in the IGT subjects, with no significant changes in HSP72. However, after the adjustment of both analyses with HOMA-IR only HSP90 difference remained significant. In conclusion, level of TRX-1 in skeletal muscle tissue was lower while that of HSP90 was higher in T2D than in IGT subjects. This may impair antioxidant defence and lead to disruptions of protein homoeostasis and redox regulation of cellular defences. Because HSP90 may be involved in sustaining functional insulin signalling pathway in type 2 diabetic muscles and higher HSP90 levels can be a consequence of type 2 diabetes, our results are potentially important for the diabetes research.</abstract><cop>Cairo, Egypt</cop><pub>Hindawi Puplishing Corporation</pub><pmid>24689038</pmid><doi>10.1155/2014/386351</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Biomedical research Blood Glucose - metabolism Diabetes Mellitus, Type 2 - metabolism Diabetes Mellitus, Type 2 - pathology Female Glucose Glucose intolerance Glucose Intolerance - metabolism Glucose Intolerance - pathology Health aspects Heat shock proteins HSP72 Heat-Shock Proteins - metabolism HSP90 Heat-Shock Proteins - metabolism Humans Insulin Kinases Male Middle Aged Muscle, Skeletal - metabolism Muscle, Skeletal - pathology Muscles Muscular system Physiological aspects Rodents Thioredoxin Thioredoxins - metabolism Type 2 diabetes |
| title | Decreased Thioredoxin-1 and Increased HSP90 Expression in Skeletal Muscle in Subjects with Type 2 Diabetes or Impaired Glucose Tolerance |
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