Selective Insulin Resistance Affecting Nitric Oxide Release But Not Plasminogen Activator Inhibitor-1 Synthesis in Fibroblasts From Insulin-Resistant Individuals
OBJECTIVES—Insulin activates several processes potentially dangerous for the arterial wall and hyperinsulinemia might be atherogenic. However, other insulin effects are protective for the vessel wall and thus anti-atherogenic. Aim of this study was to investigate whether insulin effects on potential...
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| Veröffentlicht in: | Arteriosclerosis, thrombosis, and vascular biology thrombosis, and vascular biology, 2005-11, Vol.25 (11), p.2392-2397 |
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| container_title | Arteriosclerosis, thrombosis, and vascular biology |
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| creator | Pandolfi, Assunta Solini, Anna Pellegrini, Giuliana Mincione, Gabriella Di Silvestre, Sara Chiozzi, Paola Giardinelli, Annalisa Di Marcantonio, Maria Carmela Piccirelli, Alessandro Capani, Fabio Consoli, Agostino |
| description | OBJECTIVES—Insulin activates several processes potentially dangerous for the arterial wall and hyperinsulinemia might be atherogenic. However, other insulin effects are protective for the vessel wall and thus anti-atherogenic. Aim of this study was to investigate whether insulin effects on potentially pro-atherogenic and anti-atherogenic processes were differently affected in cells from insulin-resistant individuals.
METHODS AND RESULTS—We determined insulin effect on nitric oxide (NO) production and plasminogen activator inhibitor (PAI)-1 synthesis in 12 fibroblast strains obtained from skin biopsy samples of 6 insulin-sensitive (IS) (clamp M >7 mg/kg body weight per minute) and 6 insulin-resistant (IR) (clamp M |
| doi_str_mv | 10.1161/01.ATV.0000185831.13559.a2 |
| format | Article |
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METHODS AND RESULTS—We determined insulin effect on nitric oxide (NO) production and plasminogen activator inhibitor (PAI)-1 synthesis in 12 fibroblast strains obtained from skin biopsy samples of 6 insulin-sensitive (IS) (clamp M >7 mg/kg body weight per minute) and 6 insulin-resistant (IR) (clamp M <5 mg/kg body weight per minute) healthy volunteers. Insulin effects on NO release and Akt phosphorylation were significantly impaired in fibroblasts from IR as compared with IS individuals. Conversely, there was not any difference between IR and IS strains in insulin ability to increase PAI-1 antigen levels and, after 24-hour insulin incubation, PAI-1 mRNA increase in IR strains was only slightly less than in IS strains. Insulin ability to induce MAPK activation was also comparable in IR and IS cells.
CONCLUSIONS—We conclude that in cells from IR individuals, insulin action on anti-atherogenic processes, such as NO release, is impaired, whereas the hormone ability to stimulate atherogenic processes, such as PAI-1 release, is preserved.</description><identifier>ISSN: 1079-5642</identifier><identifier>EISSN: 1524-4636</identifier><identifier>DOI: 10.1161/01.ATV.0000185831.13559.a2</identifier><identifier>PMID: 16151016</identifier><language>eng</language><publisher>United States: American Heart Association, Inc</publisher><subject>Adult ; Atherosclerosis - metabolism ; Cells, Cultured ; Culture Media ; Female ; Fibroblasts - cytology ; Fibroblasts - metabolism ; Glucose - pharmacokinetics ; Glycogen - biosynthesis ; Humans ; Hyperinsulinism - metabolism ; Insulin - pharmacology ; Insulin Resistance ; Male ; MAP Kinase Signaling System - physiology ; Nitric Oxide - metabolism ; Nitric Oxide Synthase Type III - metabolism ; Phosphorylation ; Plasminogen Activator Inhibitor 1 - genetics ; Plasminogen Activator Inhibitor 1 - metabolism ; Proto-Oncogene Proteins c-akt - metabolism ; RNA, Messenger - metabolism ; Serine - metabolism</subject><ispartof>Arteriosclerosis, thrombosis, and vascular biology, 2005-11, Vol.25 (11), p.2392-2397</ispartof><rights>2005 American Heart Association, Inc.</rights><rights>Copyright American Heart Association, Inc. Nov 2005</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4767-e1ae7ca24663eec9390c5a38f8aacd8a787c72fd0646c214cd06957a0fd75f723</citedby><cites>FETCH-LOGICAL-c4767-e1ae7ca24663eec9390c5a38f8aacd8a787c72fd0646c214cd06957a0fd75f723</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27903,27904</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16151016$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Pandolfi, Assunta</creatorcontrib><creatorcontrib>Solini, Anna</creatorcontrib><creatorcontrib>Pellegrini, Giuliana</creatorcontrib><creatorcontrib>Mincione, Gabriella</creatorcontrib><creatorcontrib>Di Silvestre, Sara</creatorcontrib><creatorcontrib>Chiozzi, Paola</creatorcontrib><creatorcontrib>Giardinelli, Annalisa</creatorcontrib><creatorcontrib>Di Marcantonio, Maria Carmela</creatorcontrib><creatorcontrib>Piccirelli, Alessandro</creatorcontrib><creatorcontrib>Capani, Fabio</creatorcontrib><creatorcontrib>Consoli, Agostino</creatorcontrib><title>Selective Insulin Resistance Affecting Nitric Oxide Release But Not Plasminogen Activator Inhibitor-1 Synthesis in Fibroblasts From Insulin-Resistant Individuals</title><title>Arteriosclerosis, thrombosis, and vascular biology</title><addtitle>Arterioscler Thromb Vasc Biol</addtitle><description>OBJECTIVES—Insulin activates several processes potentially dangerous for the arterial wall and hyperinsulinemia might be atherogenic. However, other insulin effects are protective for the vessel wall and thus anti-atherogenic. Aim of this study was to investigate whether insulin effects on potentially pro-atherogenic and anti-atherogenic processes were differently affected in cells from insulin-resistant individuals.
METHODS AND RESULTS—We determined insulin effect on nitric oxide (NO) production and plasminogen activator inhibitor (PAI)-1 synthesis in 12 fibroblast strains obtained from skin biopsy samples of 6 insulin-sensitive (IS) (clamp M >7 mg/kg body weight per minute) and 6 insulin-resistant (IR) (clamp M <5 mg/kg body weight per minute) healthy volunteers. Insulin effects on NO release and Akt phosphorylation were significantly impaired in fibroblasts from IR as compared with IS individuals. Conversely, there was not any difference between IR and IS strains in insulin ability to increase PAI-1 antigen levels and, after 24-hour insulin incubation, PAI-1 mRNA increase in IR strains was only slightly less than in IS strains. Insulin ability to induce MAPK activation was also comparable in IR and IS cells.
CONCLUSIONS—We conclude that in cells from IR individuals, insulin action on anti-atherogenic processes, such as NO release, is impaired, whereas the hormone ability to stimulate atherogenic processes, such as PAI-1 release, is preserved.</description><subject>Adult</subject><subject>Atherosclerosis - metabolism</subject><subject>Cells, Cultured</subject><subject>Culture Media</subject><subject>Female</subject><subject>Fibroblasts - cytology</subject><subject>Fibroblasts - metabolism</subject><subject>Glucose - pharmacokinetics</subject><subject>Glycogen - biosynthesis</subject><subject>Humans</subject><subject>Hyperinsulinism - metabolism</subject><subject>Insulin - pharmacology</subject><subject>Insulin Resistance</subject><subject>Male</subject><subject>MAP Kinase Signaling System - physiology</subject><subject>Nitric Oxide - metabolism</subject><subject>Nitric Oxide Synthase Type III - metabolism</subject><subject>Phosphorylation</subject><subject>Plasminogen Activator Inhibitor 1 - genetics</subject><subject>Plasminogen Activator Inhibitor 1 - metabolism</subject><subject>Proto-Oncogene Proteins c-akt - metabolism</subject><subject>RNA, Messenger - metabolism</subject><subject>Serine - metabolism</subject><issn>1079-5642</issn><issn>1524-4636</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkd1u1DAQhSMEoqXwCsjqBXcJ_rfD3VKxUKlqES3cWl5n0nVJ4mI7LX0c3hSH3aoSlqwZ29-cGflU1THBDSGSvMekWV39aHBZRAvNSEOYEG1j6bPqkAjKay6ZfF5yrNpaSE4Pqlcp3RSeU4pfVgdFRRBM5GH15xIGcNnfATqd0jz4CX2D5FO2kwO06vvlcbpG5z5H79DFb99BIQawCdDHOaPzkNHXwabRT-EaJrRaxGwOseht_caXrCbo8mHK20UXlQZrv4lhU2pyQusYxsfO9WPnXG46f-e72Q7pdfWiLwHe7ONR9X396erkS3128fn0ZHVWO66kqoFYUM5SLiUDcC1rsROW6V5b6zptlVZO0b7DkktHCXcla4WyuO-U6BVlR9W7ne5tDL9mSNmMPjkYBjtBmJORWjHNGC7g8X_gTZjjVGYztHyw1lqoAn3YQS6GlCL05jb60cYHQ7BZXDSYmOKieXLR_HPR2GWUt_sO82aE7ql0b1sB-A64D0OGmH4O8z1EswU75O0iyZnEoqYYC0LKsS6bKvYXVNWrZQ</recordid><startdate>200511</startdate><enddate>200511</enddate><creator>Pandolfi, Assunta</creator><creator>Solini, Anna</creator><creator>Pellegrini, Giuliana</creator><creator>Mincione, Gabriella</creator><creator>Di Silvestre, Sara</creator><creator>Chiozzi, Paola</creator><creator>Giardinelli, Annalisa</creator><creator>Di Marcantonio, Maria Carmela</creator><creator>Piccirelli, Alessandro</creator><creator>Capani, Fabio</creator><creator>Consoli, Agostino</creator><general>American Heart Association, 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>K9.</scope><scope>7X8</scope></search><sort><creationdate>200511</creationdate><title>Selective Insulin Resistance Affecting Nitric Oxide Release But Not Plasminogen Activator Inhibitor-1 Synthesis in Fibroblasts From Insulin-Resistant Individuals</title><author>Pandolfi, Assunta ; Solini, Anna ; Pellegrini, Giuliana ; Mincione, Gabriella ; Di Silvestre, Sara ; Chiozzi, Paola ; Giardinelli, Annalisa ; Di Marcantonio, Maria Carmela ; Piccirelli, Alessandro ; Capani, Fabio ; Consoli, Agostino</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4767-e1ae7ca24663eec9390c5a38f8aacd8a787c72fd0646c214cd06957a0fd75f723</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>Adult</topic><topic>Atherosclerosis - metabolism</topic><topic>Cells, Cultured</topic><topic>Culture Media</topic><topic>Female</topic><topic>Fibroblasts - cytology</topic><topic>Fibroblasts - metabolism</topic><topic>Glucose - pharmacokinetics</topic><topic>Glycogen - biosynthesis</topic><topic>Humans</topic><topic>Hyperinsulinism - metabolism</topic><topic>Insulin - pharmacology</topic><topic>Insulin Resistance</topic><topic>Male</topic><topic>MAP Kinase Signaling System - physiology</topic><topic>Nitric Oxide - metabolism</topic><topic>Nitric Oxide Synthase Type III - metabolism</topic><topic>Phosphorylation</topic><topic>Plasminogen Activator Inhibitor 1 - genetics</topic><topic>Plasminogen Activator Inhibitor 1 - metabolism</topic><topic>Proto-Oncogene Proteins c-akt - metabolism</topic><topic>RNA, Messenger - metabolism</topic><topic>Serine - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Pandolfi, Assunta</creatorcontrib><creatorcontrib>Solini, Anna</creatorcontrib><creatorcontrib>Pellegrini, Giuliana</creatorcontrib><creatorcontrib>Mincione, Gabriella</creatorcontrib><creatorcontrib>Di Silvestre, Sara</creatorcontrib><creatorcontrib>Chiozzi, Paola</creatorcontrib><creatorcontrib>Giardinelli, Annalisa</creatorcontrib><creatorcontrib>Di Marcantonio, Maria Carmela</creatorcontrib><creatorcontrib>Piccirelli, Alessandro</creatorcontrib><creatorcontrib>Capani, Fabio</creatorcontrib><creatorcontrib>Consoli, Agostino</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>MEDLINE - Academic</collection><jtitle>Arteriosclerosis, thrombosis, and vascular biology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Pandolfi, Assunta</au><au>Solini, Anna</au><au>Pellegrini, Giuliana</au><au>Mincione, Gabriella</au><au>Di Silvestre, Sara</au><au>Chiozzi, Paola</au><au>Giardinelli, Annalisa</au><au>Di Marcantonio, Maria Carmela</au><au>Piccirelli, Alessandro</au><au>Capani, Fabio</au><au>Consoli, Agostino</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Selective Insulin Resistance Affecting Nitric Oxide Release But Not Plasminogen Activator Inhibitor-1 Synthesis in Fibroblasts From Insulin-Resistant Individuals</atitle><jtitle>Arteriosclerosis, thrombosis, and vascular biology</jtitle><addtitle>Arterioscler Thromb Vasc Biol</addtitle><date>2005-11</date><risdate>2005</risdate><volume>25</volume><issue>11</issue><spage>2392</spage><epage>2397</epage><pages>2392-2397</pages><issn>1079-5642</issn><eissn>1524-4636</eissn><abstract>OBJECTIVES—Insulin activates several processes potentially dangerous for the arterial wall and hyperinsulinemia might be atherogenic. However, other insulin effects are protective for the vessel wall and thus anti-atherogenic. Aim of this study was to investigate whether insulin effects on potentially pro-atherogenic and anti-atherogenic processes were differently affected in cells from insulin-resistant individuals.
METHODS AND RESULTS—We determined insulin effect on nitric oxide (NO) production and plasminogen activator inhibitor (PAI)-1 synthesis in 12 fibroblast strains obtained from skin biopsy samples of 6 insulin-sensitive (IS) (clamp M >7 mg/kg body weight per minute) and 6 insulin-resistant (IR) (clamp M <5 mg/kg body weight per minute) healthy volunteers. Insulin effects on NO release and Akt phosphorylation were significantly impaired in fibroblasts from IR as compared with IS individuals. Conversely, there was not any difference between IR and IS strains in insulin ability to increase PAI-1 antigen levels and, after 24-hour insulin incubation, PAI-1 mRNA increase in IR strains was only slightly less than in IS strains. Insulin ability to induce MAPK activation was also comparable in IR and IS cells.
CONCLUSIONS—We conclude that in cells from IR individuals, insulin action on anti-atherogenic processes, such as NO release, is impaired, whereas the hormone ability to stimulate atherogenic processes, such as PAI-1 release, is preserved.</abstract><cop>United States</cop><pub>American Heart Association, Inc</pub><pmid>16151016</pmid><doi>10.1161/01.ATV.0000185831.13559.a2</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Arteriosclerosis, thrombosis, and vascular biology, 2005-11, Vol.25 (11), p.2392-2397 |
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| source | MEDLINE; Journals@Ovid Ovid Autoload; Alma/SFX Local Collection |
| subjects | Adult Atherosclerosis - metabolism Cells, Cultured Culture Media Female Fibroblasts - cytology Fibroblasts - metabolism Glucose - pharmacokinetics Glycogen - biosynthesis Humans Hyperinsulinism - metabolism Insulin - pharmacology Insulin Resistance Male MAP Kinase Signaling System - physiology Nitric Oxide - metabolism Nitric Oxide Synthase Type III - metabolism Phosphorylation Plasminogen Activator Inhibitor 1 - genetics Plasminogen Activator Inhibitor 1 - metabolism Proto-Oncogene Proteins c-akt - metabolism RNA, Messenger - metabolism Serine - metabolism |
| title | Selective Insulin Resistance Affecting Nitric Oxide Release But Not Plasminogen Activator Inhibitor-1 Synthesis in Fibroblasts From Insulin-Resistant Individuals |
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