Effects of diabetes, vanadium, and insulin on glycogen synthase activation in Wistar rats
In vivo effects of insulin and vanadium treatment on glycogen synthase (GS), glycogen synthase kinase-3 (GSK-3) and protein phosphatase-1 (PP1) activity were determined in Wistar rats with streptozotocin (STZ)-induced diabetes. The skeletal muscle was freeze-clamped before or following an insulin in...
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| Veröffentlicht in: | Molecular and cellular biochemistry 2002-02, Vol.231 (1-2), p.23-35 |
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| creator | Semiz, Sabina Orvig, Chris McNeill, John H |
| description | In vivo effects of insulin and vanadium treatment on glycogen synthase (GS), glycogen synthase kinase-3 (GSK-3) and protein phosphatase-1 (PP1) activity were determined in Wistar rats with streptozotocin (STZ)-induced diabetes. The skeletal muscle was freeze-clamped before or following an insulin injection (5 U/kg i.v.). Diabetes, vanadium, and insulin in vivo treatment did not affect muscle GSK-3beta activity as compared to controls. Following insulin stimulation in 4-week STZ-diabetic rats muscle GS fractional activity (GSFA) was increased 3 fold (p < 0.05), while in 7-week diabetic rats it remained unchanged, suggesting development of insulin resistance in longer term diabetes. Muscle PP1 activity was increased in diabetic rats and returned to normal after vanadium treatment, while muscle GSFA remained unchanged. Therefore, it is possible that PP1 is involved in the regulation of some other cellular events of vanadium (other than regulation of glycogen synthesis). The lack of effect of vanadium treatment in stimulating glycogen synthesis in skeletal muscle suggests the involvement of other metabolic pathways in the observed glucoregulatory effect of vanadium. |
| doi_str_mv | 10.1023/A:1014437019586 |
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The skeletal muscle was freeze-clamped before or following an insulin injection (5 U/kg i.v.). Diabetes, vanadium, and insulin in vivo treatment did not affect muscle GSK-3beta activity as compared to controls. Following insulin stimulation in 4-week STZ-diabetic rats muscle GS fractional activity (GSFA) was increased 3 fold (p < 0.05), while in 7-week diabetic rats it remained unchanged, suggesting development of insulin resistance in longer term diabetes. Muscle PP1 activity was increased in diabetic rats and returned to normal after vanadium treatment, while muscle GSFA remained unchanged. Therefore, it is possible that PP1 is involved in the regulation of some other cellular events of vanadium (other than regulation of glycogen synthesis). The lack of effect of vanadium treatment in stimulating glycogen synthesis in skeletal muscle suggests the involvement of other metabolic pathways in the observed glucoregulatory effect of vanadium.</description><identifier>ISSN: 0300-8177</identifier><identifier>EISSN: 1573-4919</identifier><identifier>DOI: 10.1023/A:1014437019586</identifier><identifier>PMID: 11952162</identifier><language>eng</language><publisher>Netherlands: Springer Nature B.V</publisher><subject>Animals ; Blood Glucose ; Diabetes ; Diabetes Mellitus - enzymology ; Enzyme Activation - drug effects ; Glycogen Synthase - metabolism ; Glycogen Synthase Kinase 3 - metabolism ; Insulin - blood ; Insulin - pharmacology ; Insulin resistance ; Muscle, Skeletal - enzymology ; Phosphoprotein Phosphatases - metabolism ; Protein Phosphatase 1 ; Rats ; Rats, Wistar ; Rodents ; Time Factors ; Vanadium ; Vanadium - pharmacology</subject><ispartof>Molecular and cellular biochemistry, 2002-02, Vol.231 (1-2), p.23-35</ispartof><rights>Kluwer Academic Publishers 2002</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c280t-ba5b3dd18bb92f5d41a69387bcc924aeddbadb4c25d7a28c10c8d40ec21232903</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27923,27924</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/11952162$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Semiz, Sabina</creatorcontrib><creatorcontrib>Orvig, Chris</creatorcontrib><creatorcontrib>McNeill, John H</creatorcontrib><title>Effects of diabetes, vanadium, and insulin on glycogen synthase activation in Wistar rats</title><title>Molecular and cellular biochemistry</title><addtitle>Mol Cell Biochem</addtitle><description>In vivo effects of insulin and vanadium treatment on glycogen synthase (GS), glycogen synthase kinase-3 (GSK-3) and protein phosphatase-1 (PP1) activity were determined in Wistar rats with streptozotocin (STZ)-induced diabetes. The skeletal muscle was freeze-clamped before or following an insulin injection (5 U/kg i.v.). Diabetes, vanadium, and insulin in vivo treatment did not affect muscle GSK-3beta activity as compared to controls. Following insulin stimulation in 4-week STZ-diabetic rats muscle GS fractional activity (GSFA) was increased 3 fold (p < 0.05), while in 7-week diabetic rats it remained unchanged, suggesting development of insulin resistance in longer term diabetes. Muscle PP1 activity was increased in diabetic rats and returned to normal after vanadium treatment, while muscle GSFA remained unchanged. Therefore, it is possible that PP1 is involved in the regulation of some other cellular events of vanadium (other than regulation of glycogen synthesis). The lack of effect of vanadium treatment in stimulating glycogen synthesis in skeletal muscle suggests the involvement of other metabolic pathways in the observed glucoregulatory effect of vanadium.</description><subject>Animals</subject><subject>Blood Glucose</subject><subject>Diabetes</subject><subject>Diabetes Mellitus - enzymology</subject><subject>Enzyme Activation - drug effects</subject><subject>Glycogen Synthase - metabolism</subject><subject>Glycogen Synthase Kinase 3 - metabolism</subject><subject>Insulin - blood</subject><subject>Insulin - pharmacology</subject><subject>Insulin resistance</subject><subject>Muscle, Skeletal - enzymology</subject><subject>Phosphoprotein Phosphatases - metabolism</subject><subject>Protein Phosphatase 1</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Rodents</subject><subject>Time Factors</subject><subject>Vanadium</subject><subject>Vanadium - pharmacology</subject><issn>0300-8177</issn><issn>1573-4919</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2002</creationdate><recordtype>article</recordtype><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>eNpd0MtLAzEQBvAgiq3VszcJHjx1NZPsI-utlPqAghdFPC2Tx9aU3axusoX-9y5YL8LAHL4fw8cQcgnsFhgXd4t7YJCmomBQZjI_IlPICpGkJZTHZMoEY4mEopiQsxC2jME4cEomMGoOOZ-Sj1VdWx0D7WpqHCobbZjTHXo0bmjnFL2hzoehcZ52nm6ave421tOw9_ETg6Woo9thdGM4kncXIva0xxjOyUmNTbAXhz0jbw-r1-VTsn55fF4u1onmksVEYaaEMSCVKnmdmRQwL4UslNYlT9Eao9CoVPPMFMilBqalSZnVHLjgJRMzcvN796vvvgcbYtW6oG3ToLfdEKoCcgYy5yO8_ge33dD7sVtVZDlP89GM6OqABtVaU331rsV-X_19TPwA_9xtYA</recordid><startdate>20020201</startdate><enddate>20020201</enddate><creator>Semiz, Sabina</creator><creator>Orvig, Chris</creator><creator>McNeill, John H</creator><general>Springer Nature B.V</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>3V.</scope><scope>7QL</scope><scope>7QP</scope><scope>7T5</scope><scope>7T7</scope><scope>7TK</scope><scope>7TM</scope><scope>7TO</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>88I</scope><scope>8AO</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AEUYN</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>M2P</scope><scope>M7N</scope><scope>M7P</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>20020201</creationdate><title>Effects of diabetes, vanadium, and insulin on glycogen synthase activation in Wistar rats</title><author>Semiz, Sabina ; Orvig, Chris ; McNeill, John H</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c280t-ba5b3dd18bb92f5d41a69387bcc924aeddbadb4c25d7a28c10c8d40ec21232903</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2002</creationdate><topic>Animals</topic><topic>Blood Glucose</topic><topic>Diabetes</topic><topic>Diabetes Mellitus - enzymology</topic><topic>Enzyme Activation - drug effects</topic><topic>Glycogen Synthase - metabolism</topic><topic>Glycogen Synthase Kinase 3 - metabolism</topic><topic>Insulin - blood</topic><topic>Insulin - pharmacology</topic><topic>Insulin resistance</topic><topic>Muscle, Skeletal - enzymology</topic><topic>Phosphoprotein Phosphatases - metabolism</topic><topic>Protein Phosphatase 1</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Rodents</topic><topic>Time Factors</topic><topic>Vanadium</topic><topic>Vanadium - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Semiz, Sabina</creatorcontrib><creatorcontrib>Orvig, Chris</creatorcontrib><creatorcontrib>McNeill, John H</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>ProQuest Central (Corporate)</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Immunology Abstracts</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Oncogenes and Growth Factors 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>Science Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research Database</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 One Sustainability</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>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</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>Science Database</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</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 Basic</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Molecular and cellular biochemistry</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Semiz, Sabina</au><au>Orvig, Chris</au><au>McNeill, John H</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Effects of diabetes, vanadium, and insulin on glycogen synthase activation in Wistar rats</atitle><jtitle>Molecular and cellular biochemistry</jtitle><addtitle>Mol Cell Biochem</addtitle><date>2002-02-01</date><risdate>2002</risdate><volume>231</volume><issue>1-2</issue><spage>23</spage><epage>35</epage><pages>23-35</pages><issn>0300-8177</issn><eissn>1573-4919</eissn><abstract>In vivo effects of insulin and vanadium treatment on glycogen synthase (GS), glycogen synthase kinase-3 (GSK-3) and protein phosphatase-1 (PP1) activity were determined in Wistar rats with streptozotocin (STZ)-induced diabetes. The skeletal muscle was freeze-clamped before or following an insulin injection (5 U/kg i.v.). Diabetes, vanadium, and insulin in vivo treatment did not affect muscle GSK-3beta activity as compared to controls. Following insulin stimulation in 4-week STZ-diabetic rats muscle GS fractional activity (GSFA) was increased 3 fold (p < 0.05), while in 7-week diabetic rats it remained unchanged, suggesting development of insulin resistance in longer term diabetes. Muscle PP1 activity was increased in diabetic rats and returned to normal after vanadium treatment, while muscle GSFA remained unchanged. Therefore, it is possible that PP1 is involved in the regulation of some other cellular events of vanadium (other than regulation of glycogen synthesis). The lack of effect of vanadium treatment in stimulating glycogen synthesis in skeletal muscle suggests the involvement of other metabolic pathways in the observed glucoregulatory effect of vanadium.</abstract><cop>Netherlands</cop><pub>Springer Nature B.V</pub><pmid>11952162</pmid><doi>10.1023/A:1014437019586</doi><tpages>13</tpages></addata></record> |
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| subjects | Animals Blood Glucose Diabetes Diabetes Mellitus - enzymology Enzyme Activation - drug effects Glycogen Synthase - metabolism Glycogen Synthase Kinase 3 - metabolism Insulin - blood Insulin - pharmacology Insulin resistance Muscle, Skeletal - enzymology Phosphoprotein Phosphatases - metabolism Protein Phosphatase 1 Rats Rats, Wistar Rodents Time Factors Vanadium Vanadium - pharmacology |
| title | Effects of diabetes, vanadium, and insulin on glycogen synthase activation in Wistar rats |
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