Insulin hyperresponsiveness in partially hepatectomized diabetic rats
The present work analyzes the expression of insulin receptors and theirs related intracellular signaling molecules in partially hepatectomized-diabetic rats. Insulin binding through Scatchard analysis was studied using isolated hepatocytes of Control (Sham-operated), Hepatectomized, Diabetic and Dia...
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| Veröffentlicht in: | Life sciences (1973) 2001-02, Vol.68 (12), p.1417-1426 |
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| container_title | Life sciences (1973) |
| container_volume | 68 |
| creator | Carrillo, Marı́a C. Favre, Cristián Monti, Juan A. Alvarez, Marı́a L. Carnovale, Cristina E. |
| description | The present work analyzes the expression of insulin receptors and theirs related intracellular signaling molecules in partially hepatectomized-diabetic rats. Insulin binding through Scatchard analysis was studied using isolated hepatocytes of Control (Sham-operated), Hepatectomized, Diabetic and Diabetic-Hepatectomized male Wistar rats. In a set of
in vivo experiments, the levels of α subunit of the insulin receptor, the insulin receptor substrate 1 (IRS-1) and the phosphatidylinositol 3-kinase (PI3K) were determined. [
3H]-thymidine incorporation into DNA 24 or 48 h after surgery was assessed in all the experimental groups. Scatchard analysis showed that insulin receptor number was increased in diabetic and in hepatectomized rats in the same extent (64%, with respect to Controls). Diabetic-hepatectomized rats showed a dramatic increase of the receptor concentration (400%) and on the affinity constant (532%). Besides, the insulin receptor expression was increased in the treated groups, being the higher values those of the diabetic-hepatectomized rats. IRS-1 and PI3K showed similar increases. DNA synthesis was not impaired by the diabetes state. In conclusion, increased expression of IR and IRS-1 leads to increased association of PI3K
in vivo in diabetic regenerating rats. The enhancement of this pathway may reveal an insulin hyperresponsiveness in these animals. |
| doi_str_mv | 10.1016/S0024-3205(01)00936-5 |
| format | Article |
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in vivo experiments, the levels of α subunit of the insulin receptor, the insulin receptor substrate 1 (IRS-1) and the phosphatidylinositol 3-kinase (PI3K) were determined. [
3H]-thymidine incorporation into DNA 24 or 48 h after surgery was assessed in all the experimental groups. Scatchard analysis showed that insulin receptor number was increased in diabetic and in hepatectomized rats in the same extent (64%, with respect to Controls). Diabetic-hepatectomized rats showed a dramatic increase of the receptor concentration (400%) and on the affinity constant (532%). Besides, the insulin receptor expression was increased in the treated groups, being the higher values those of the diabetic-hepatectomized rats. IRS-1 and PI3K showed similar increases. DNA synthesis was not impaired by the diabetes state. In conclusion, increased expression of IR and IRS-1 leads to increased association of PI3K
in vivo in diabetic regenerating rats. The enhancement of this pathway may reveal an insulin hyperresponsiveness in these animals.</description><identifier>ISSN: 0024-3205</identifier><identifier>EISSN: 1879-0631</identifier><identifier>DOI: 10.1016/S0024-3205(01)00936-5</identifier><identifier>PMID: 11388693</identifier><language>eng</language><publisher>Netherlands: Elsevier Inc</publisher><subject>Animals ; Binding Sites ; Binding, Competitive ; Cell Count ; Cell Survival ; Diabetes ; Diabetes Mellitus, Experimental - drug therapy ; Diabetes Mellitus, Experimental - metabolism ; DNA - biosynthesis ; Hepatectomy ; Hepatocytes - cytology ; Hepatocytes - metabolism ; In Vitro Techniques ; Insulin ; Insulin - metabolism ; Insulin - pharmacology ; Insulin intracellular pathways ; Insulin Receptor Substrate Proteins ; Insulin receptors ; Liver Regeneration ; Male ; Phosphatidylinositol 3-Kinases - metabolism ; Phosphoproteins - metabolism ; Rats ; Rats, Wistar ; Receptor, Insulin - metabolism</subject><ispartof>Life sciences (1973), 2001-02, Vol.68 (12), p.1417-1426</ispartof><rights>2001 Elsevier Science Inc.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c361t-8c3bd84469a65497bc5bbcbcc4efda583c852f637667cf9589314bf54b317f353</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/S0024-3205(01)00936-5$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>315,781,785,3551,27929,27930,46000</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/11388693$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Carrillo, Marı́a C.</creatorcontrib><creatorcontrib>Favre, Cristián</creatorcontrib><creatorcontrib>Monti, Juan A.</creatorcontrib><creatorcontrib>Alvarez, Marı́a L.</creatorcontrib><creatorcontrib>Carnovale, Cristina E.</creatorcontrib><title>Insulin hyperresponsiveness in partially hepatectomized diabetic rats</title><title>Life sciences (1973)</title><addtitle>Life Sci</addtitle><description>The present work analyzes the expression of insulin receptors and theirs related intracellular signaling molecules in partially hepatectomized-diabetic rats. Insulin binding through Scatchard analysis was studied using isolated hepatocytes of Control (Sham-operated), Hepatectomized, Diabetic and Diabetic-Hepatectomized male Wistar rats. In a set of
in vivo experiments, the levels of α subunit of the insulin receptor, the insulin receptor substrate 1 (IRS-1) and the phosphatidylinositol 3-kinase (PI3K) were determined. [
3H]-thymidine incorporation into DNA 24 or 48 h after surgery was assessed in all the experimental groups. Scatchard analysis showed that insulin receptor number was increased in diabetic and in hepatectomized rats in the same extent (64%, with respect to Controls). Diabetic-hepatectomized rats showed a dramatic increase of the receptor concentration (400%) and on the affinity constant (532%). Besides, the insulin receptor expression was increased in the treated groups, being the higher values those of the diabetic-hepatectomized rats. IRS-1 and PI3K showed similar increases. DNA synthesis was not impaired by the diabetes state. In conclusion, increased expression of IR and IRS-1 leads to increased association of PI3K
in vivo in diabetic regenerating rats. The enhancement of this pathway may reveal an insulin hyperresponsiveness in these animals.</description><subject>Animals</subject><subject>Binding Sites</subject><subject>Binding, Competitive</subject><subject>Cell Count</subject><subject>Cell Survival</subject><subject>Diabetes</subject><subject>Diabetes Mellitus, Experimental - drug therapy</subject><subject>Diabetes Mellitus, Experimental - metabolism</subject><subject>DNA - biosynthesis</subject><subject>Hepatectomy</subject><subject>Hepatocytes - cytology</subject><subject>Hepatocytes - metabolism</subject><subject>In Vitro Techniques</subject><subject>Insulin</subject><subject>Insulin - metabolism</subject><subject>Insulin - pharmacology</subject><subject>Insulin intracellular pathways</subject><subject>Insulin Receptor Substrate Proteins</subject><subject>Insulin receptors</subject><subject>Liver Regeneration</subject><subject>Male</subject><subject>Phosphatidylinositol 3-Kinases - metabolism</subject><subject>Phosphoproteins - metabolism</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Receptor, Insulin - metabolism</subject><issn>0024-3205</issn><issn>1879-0631</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2001</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkE1LAzEQhoMotlZ_grIn0cNq0myyyUmkVC0UPKjnkGRnaWS_TLKF-uvdfqBHTwPD887LPAhdEnxHMOH3bxhPs5ROMbvB5BZjSXnKjtCYiFymmFNyjMa_yAidhfCJMWYsp6doRAgVgks6RvNFE_rKNclq04H3ELq2CW4NDYSQDOtO--h0VW2SFXQ6go1t7b6hSAqnDURnE69jOEcnpa4CXBzmBH08zd9nL-ny9Xkxe1ymlnISU2GpKUSWcak5y2RuLDPGGmszKAvNBLWCTUtOc85zW0omJCWZKVlmKMlLyugEXe_vdr796iFEVbtgoap0A20fVI7FkGJyANketL4NwUOpOu9q7TeKYLX1p3b-1FaOwkTt_KltwdWhoDc1FH-pg7ABeNgDMLy5duBVsA4aC4XzgxxVtO6fih-8w4CU</recordid><startdate>20010209</startdate><enddate>20010209</enddate><creator>Carrillo, Marı́a C.</creator><creator>Favre, Cristián</creator><creator>Monti, Juan A.</creator><creator>Alvarez, Marı́a L.</creator><creator>Carnovale, Cristina E.</creator><general>Elsevier Inc</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>20010209</creationdate><title>Insulin hyperresponsiveness in partially hepatectomized diabetic rats</title><author>Carrillo, Marı́a C. ; Favre, Cristián ; Monti, Juan A. ; Alvarez, Marı́a L. ; Carnovale, Cristina E.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c361t-8c3bd84469a65497bc5bbcbcc4efda583c852f637667cf9589314bf54b317f353</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2001</creationdate><topic>Animals</topic><topic>Binding Sites</topic><topic>Binding, Competitive</topic><topic>Cell Count</topic><topic>Cell Survival</topic><topic>Diabetes</topic><topic>Diabetes Mellitus, Experimental - drug therapy</topic><topic>Diabetes Mellitus, Experimental - metabolism</topic><topic>DNA - biosynthesis</topic><topic>Hepatectomy</topic><topic>Hepatocytes - cytology</topic><topic>Hepatocytes - metabolism</topic><topic>In Vitro Techniques</topic><topic>Insulin</topic><topic>Insulin - metabolism</topic><topic>Insulin - pharmacology</topic><topic>Insulin intracellular pathways</topic><topic>Insulin Receptor Substrate Proteins</topic><topic>Insulin receptors</topic><topic>Liver Regeneration</topic><topic>Male</topic><topic>Phosphatidylinositol 3-Kinases - metabolism</topic><topic>Phosphoproteins - metabolism</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Receptor, Insulin - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Carrillo, Marı́a C.</creatorcontrib><creatorcontrib>Favre, Cristián</creatorcontrib><creatorcontrib>Monti, Juan A.</creatorcontrib><creatorcontrib>Alvarez, Marı́a L.</creatorcontrib><creatorcontrib>Carnovale, Cristina E.</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>Life sciences (1973)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Carrillo, Marı́a C.</au><au>Favre, Cristián</au><au>Monti, Juan A.</au><au>Alvarez, Marı́a L.</au><au>Carnovale, Cristina E.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Insulin hyperresponsiveness in partially hepatectomized diabetic rats</atitle><jtitle>Life sciences (1973)</jtitle><addtitle>Life Sci</addtitle><date>2001-02-09</date><risdate>2001</risdate><volume>68</volume><issue>12</issue><spage>1417</spage><epage>1426</epage><pages>1417-1426</pages><issn>0024-3205</issn><eissn>1879-0631</eissn><abstract>The present work analyzes the expression of insulin receptors and theirs related intracellular signaling molecules in partially hepatectomized-diabetic rats. Insulin binding through Scatchard analysis was studied using isolated hepatocytes of Control (Sham-operated), Hepatectomized, Diabetic and Diabetic-Hepatectomized male Wistar rats. In a set of
in vivo experiments, the levels of α subunit of the insulin receptor, the insulin receptor substrate 1 (IRS-1) and the phosphatidylinositol 3-kinase (PI3K) were determined. [
3H]-thymidine incorporation into DNA 24 or 48 h after surgery was assessed in all the experimental groups. Scatchard analysis showed that insulin receptor number was increased in diabetic and in hepatectomized rats in the same extent (64%, with respect to Controls). Diabetic-hepatectomized rats showed a dramatic increase of the receptor concentration (400%) and on the affinity constant (532%). Besides, the insulin receptor expression was increased in the treated groups, being the higher values those of the diabetic-hepatectomized rats. IRS-1 and PI3K showed similar increases. DNA synthesis was not impaired by the diabetes state. In conclusion, increased expression of IR and IRS-1 leads to increased association of PI3K
in vivo in diabetic regenerating rats. The enhancement of this pathway may reveal an insulin hyperresponsiveness in these animals.</abstract><cop>Netherlands</cop><pub>Elsevier Inc</pub><pmid>11388693</pmid><doi>10.1016/S0024-3205(01)00936-5</doi><tpages>10</tpages></addata></record> |
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| source | MEDLINE; Elsevier ScienceDirect Journals Complete |
| subjects | Animals Binding Sites Binding, Competitive Cell Count Cell Survival Diabetes Diabetes Mellitus, Experimental - drug therapy Diabetes Mellitus, Experimental - metabolism DNA - biosynthesis Hepatectomy Hepatocytes - cytology Hepatocytes - metabolism In Vitro Techniques Insulin Insulin - metabolism Insulin - pharmacology Insulin intracellular pathways Insulin Receptor Substrate Proteins Insulin receptors Liver Regeneration Male Phosphatidylinositol 3-Kinases - metabolism Phosphoproteins - metabolism Rats Rats, Wistar Receptor, Insulin - metabolism |
| title | Insulin hyperresponsiveness in partially hepatectomized diabetic rats |
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