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Treatment with a copper-selective chelator causes substantive improvement in cardiac function of diabetic rats with left-ventricular impairment
Defective copper regulation is implicated as a causative mechanism of organ damage in diabetes. Treatment with trientine, a divalent-copper-selective chelator, improves arterial and renal structure/function in diabetes, wherein it also ameliorates left-ventricular (LV) hypertrophy. However, direct i...
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| Published in: | Cardiovascular diabetology 2013-01, Vol.12 (1), p.28-28, Article 28 |
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| container_title | Cardiovascular diabetology |
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| creator | Lu, Jun Pontré, Beau Pickup, Stephen Choong, Soon Y Li, Mingming Xu, Hong Gamble, Gregory D Phillips, Anthony R J Cowan, Brett R Young, Alistair A Cooper, Garth J S |
| description | Defective copper regulation is implicated as a causative mechanism of organ damage in diabetes. Treatment with trientine, a divalent-copper-selective chelator, improves arterial and renal structure/function in diabetes, wherein it also ameliorates left-ventricular (LV) hypertrophy. However, direct in vivo evidence that trientine can improve cardiac function in heart failure has hitherto been lacking.
To determine whether trientine treatment could improve in vivo outcome, we measured cardiac function in groups of trientine-treated diabetic (TETA-DIA), non-drug-treated diabetic (DIA) and sham-treated control (SHAM) rats, by using in vivo high-field cardiac magnetic-resonance imaging (cMRI) and an ex vivo isolated-perfused working heart method. Forty age-matched animals underwent a cMRI scan after which 12 were randomized to the SHAM group and 28 underwent streptozotocin-injection; of these, 25 developed stable diabetes, and 12 were then randomized to receive no treatment for 16 weeks (DIA) and the other 13 to undergo 8-weeks' untreated diabetes followed by 8-weeks' drug treatment (TETA-DIA). Animals were studied again by cMRI at 8 and 16 weeks following disease induction, and finally by measurement of ex vivo cardiac function.
After eight weeks diabetes, rats (DIA/TETA-DIA) had developed significant impairment of LV function, as judged by impairment of ejection fraction (LVEF), cardiac output (CO), and LV mass (LVM)/body-mass (all P |
| doi_str_mv | 10.1186/1475-2840-12-28 |
| format | article |
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To determine whether trientine treatment could improve in vivo outcome, we measured cardiac function in groups of trientine-treated diabetic (TETA-DIA), non-drug-treated diabetic (DIA) and sham-treated control (SHAM) rats, by using in vivo high-field cardiac magnetic-resonance imaging (cMRI) and an ex vivo isolated-perfused working heart method. Forty age-matched animals underwent a cMRI scan after which 12 were randomized to the SHAM group and 28 underwent streptozotocin-injection; of these, 25 developed stable diabetes, and 12 were then randomized to receive no treatment for 16 weeks (DIA) and the other 13 to undergo 8-weeks' untreated diabetes followed by 8-weeks' drug treatment (TETA-DIA). Animals were studied again by cMRI at 8 and 16 weeks following disease induction, and finally by measurement of ex vivo cardiac function.
After eight weeks diabetes, rats (DIA/TETA-DIA) had developed significant impairment of LV function, as judged by impairment of ejection fraction (LVEF), cardiac output (CO), and LV mass (LVM)/body-mass (all P < 0.001), as well as other functional indexes. LVEF, CO (both P < 0.001) and the other indexes deteriorated further at 16 weeks in DIA, whereas trientine (TETA-DIA) improved cardiac function by elevating LVEF and CO (both P < 0.001), and also partially reversed the increase in LVM/body-mass (P < 0.05). In ex vivo hearts from DIA, the CO response to increasing preload pressure was deficient compared with SHAM (P < 0.001) whereas the preload-CO relationship was significantly improved in TETA-DIA animals (P < 0.001).
Trientine treatment significantly improved cardiac function in diabetic rats with substantive LV impairment. These results implicate impaired copper regulation in the pathogenesis of impaired cardiac function caused by diabetic cardiomyopathy, and support ongoing studies of trientine treatment in patients with heart failure.]]></description><identifier>ISSN: 1475-2840</identifier><identifier>EISSN: 1475-2840</identifier><identifier>DOI: 10.1186/1475-2840-12-28</identifier><identifier>PMID: 23368770</identifier><language>eng</language><publisher>England: BioMed Central</publisher><subject>Animals ; Chelating Agents - pharmacology ; Chelating Agents - therapeutic use ; Copper ; Diabetes ; Diabetes Mellitus, Experimental - drug therapy ; Diabetes Mellitus, Experimental - physiopathology ; Heart - drug effects ; Heart - physiology ; Heart failure ; Heart Function Tests ; Male ; Medical research ; Metabolic disorders ; Original Investigation ; Rats ; Rats, Wistar ; Rodents ; Treatment Outcome ; Trientine - pharmacology ; Trientine - therapeutic use ; Ventricular Dysfunction, Left - drug therapy ; Ventricular Dysfunction, Left - physiopathology</subject><ispartof>Cardiovascular diabetology, 2013-01, Vol.12 (1), p.28-28, Article 28</ispartof><rights>2013 Lu et al.; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.</rights><rights>Copyright ©2013 Lu et al.; licensee BioMed Central Ltd. 2013 Lu et al.; licensee BioMed Central Ltd.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c488t-80086c695674eb70049e3bc4125ce930041bba1dba5faafb672e030674c42b673</citedby><cites>FETCH-LOGICAL-c488t-80086c695674eb70049e3bc4125ce930041bba1dba5faafb672e030674c42b673</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/PMC3602174/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.proquest.com/docview/1317665653?pq-origsite=primo$$EHTML$$P50$$Gproquest$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,25752,27923,27924,37011,37012,44589,53790,53792</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23368770$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lu, Jun</creatorcontrib><creatorcontrib>Pontré, Beau</creatorcontrib><creatorcontrib>Pickup, Stephen</creatorcontrib><creatorcontrib>Choong, Soon Y</creatorcontrib><creatorcontrib>Li, Mingming</creatorcontrib><creatorcontrib>Xu, Hong</creatorcontrib><creatorcontrib>Gamble, Gregory D</creatorcontrib><creatorcontrib>Phillips, Anthony R J</creatorcontrib><creatorcontrib>Cowan, Brett R</creatorcontrib><creatorcontrib>Young, Alistair A</creatorcontrib><creatorcontrib>Cooper, Garth J S</creatorcontrib><title>Treatment with a copper-selective chelator causes substantive improvement in cardiac function of diabetic rats with left-ventricular impairment</title><title>Cardiovascular diabetology</title><addtitle>Cardiovasc Diabetol</addtitle><description><![CDATA[Defective copper regulation is implicated as a causative mechanism of organ damage in diabetes. Treatment with trientine, a divalent-copper-selective chelator, improves arterial and renal structure/function in diabetes, wherein it also ameliorates left-ventricular (LV) hypertrophy. However, direct in vivo evidence that trientine can improve cardiac function in heart failure has hitherto been lacking.
To determine whether trientine treatment could improve in vivo outcome, we measured cardiac function in groups of trientine-treated diabetic (TETA-DIA), non-drug-treated diabetic (DIA) and sham-treated control (SHAM) rats, by using in vivo high-field cardiac magnetic-resonance imaging (cMRI) and an ex vivo isolated-perfused working heart method. Forty age-matched animals underwent a cMRI scan after which 12 were randomized to the SHAM group and 28 underwent streptozotocin-injection; of these, 25 developed stable diabetes, and 12 were then randomized to receive no treatment for 16 weeks (DIA) and the other 13 to undergo 8-weeks' untreated diabetes followed by 8-weeks' drug treatment (TETA-DIA). Animals were studied again by cMRI at 8 and 16 weeks following disease induction, and finally by measurement of ex vivo cardiac function.
After eight weeks diabetes, rats (DIA/TETA-DIA) had developed significant impairment of LV function, as judged by impairment of ejection fraction (LVEF), cardiac output (CO), and LV mass (LVM)/body-mass (all P < 0.001), as well as other functional indexes. LVEF, CO (both P < 0.001) and the other indexes deteriorated further at 16 weeks in DIA, whereas trientine (TETA-DIA) improved cardiac function by elevating LVEF and CO (both P < 0.001), and also partially reversed the increase in LVM/body-mass (P < 0.05). In ex vivo hearts from DIA, the CO response to increasing preload pressure was deficient compared with SHAM (P < 0.001) whereas the preload-CO relationship was significantly improved in TETA-DIA animals (P < 0.001).
Trientine treatment significantly improved cardiac function in diabetic rats with substantive LV impairment. These results implicate impaired copper regulation in the pathogenesis of impaired cardiac function caused by diabetic cardiomyopathy, and support ongoing studies of trientine treatment in patients with heart failure.]]></description><subject>Animals</subject><subject>Chelating Agents - pharmacology</subject><subject>Chelating Agents - therapeutic use</subject><subject>Copper</subject><subject>Diabetes</subject><subject>Diabetes Mellitus, Experimental - drug therapy</subject><subject>Diabetes Mellitus, Experimental - physiopathology</subject><subject>Heart - drug effects</subject><subject>Heart - physiology</subject><subject>Heart failure</subject><subject>Heart Function Tests</subject><subject>Male</subject><subject>Medical research</subject><subject>Metabolic disorders</subject><subject>Original Investigation</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Rodents</subject><subject>Treatment Outcome</subject><subject>Trientine - pharmacology</subject><subject>Trientine - therapeutic use</subject><subject>Ventricular Dysfunction, Left - drug therapy</subject><subject>Ventricular Dysfunction, Left - physiopathology</subject><issn>1475-2840</issn><issn>1475-2840</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>PIMPY</sourceid><recordid>eNpdkU1v1DAQhi1ERUvLmRuyxIVLqL9iZy9IqOJLqtRLe7bG3gnrKomD7SziV_CXcbplVTiNZ-aZ1zN6CXnN2XvOO33JlWkb0SnWcFHjM3J2rDx_8j4lL3O-Z4ybTvMX5FRIqTtj2Bn5fZsQyohToT9D2VGgPs4zpibjgL6EPVK_wwFKTNTDkjHTvLhcYHrohXFOcY8P82GqRNoG8LRfpjobJxp7WgsOS_A0QcmHTwbsS7OvMyn4ZYC0ykBIq8oFOelhyPjqMZ6Tu8-fbq--Ntc3X75dfbxuvOq60nSMddrrTauNQmcYUxuUzisuWo8bWXPuHPCtg7YH6J02AplklfZK1Eyekw8H3XlxI279ugwMdk5hhPTLRgj2384UdvZ73FupmeBGVYF3jwIp_lgwFzuG7HEYYMK4ZMul4FIqwUVF3_6H3sclTfW8SnGjdatbWanLA-VTzDlhf1yGM7uabVc77Wqn5aLGOvHm6Q1H_q-78g-mM6iK</recordid><startdate>20130131</startdate><enddate>20130131</enddate><creator>Lu, Jun</creator><creator>Pontré, Beau</creator><creator>Pickup, Stephen</creator><creator>Choong, Soon Y</creator><creator>Li, Mingming</creator><creator>Xu, Hong</creator><creator>Gamble, Gregory D</creator><creator>Phillips, Anthony R J</creator><creator>Cowan, Brett R</creator><creator>Young, Alistair A</creator><creator>Cooper, Garth J S</creator><general>BioMed Central</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>3V.</scope><scope>7T5</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>H94</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</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>20130131</creationdate><title>Treatment with a copper-selective chelator causes substantive improvement in cardiac function of diabetic rats with left-ventricular impairment</title><author>Lu, Jun ; Pontré, Beau ; Pickup, Stephen ; Choong, Soon Y ; Li, Mingming ; Xu, Hong ; Gamble, Gregory D ; Phillips, Anthony R J ; Cowan, Brett R ; Young, Alistair A ; Cooper, Garth J S</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c488t-80086c695674eb70049e3bc4125ce930041bba1dba5faafb672e030674c42b673</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>Animals</topic><topic>Chelating Agents - pharmacology</topic><topic>Chelating Agents - therapeutic use</topic><topic>Copper</topic><topic>Diabetes</topic><topic>Diabetes Mellitus, Experimental - drug therapy</topic><topic>Diabetes Mellitus, Experimental - physiopathology</topic><topic>Heart - drug effects</topic><topic>Heart - physiology</topic><topic>Heart failure</topic><topic>Heart Function Tests</topic><topic>Male</topic><topic>Medical research</topic><topic>Metabolic disorders</topic><topic>Original Investigation</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Rodents</topic><topic>Treatment Outcome</topic><topic>Trientine - pharmacology</topic><topic>Trientine - therapeutic use</topic><topic>Ventricular Dysfunction, Left - drug therapy</topic><topic>Ventricular Dysfunction, Left - physiopathology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Lu, Jun</creatorcontrib><creatorcontrib>Pontré, Beau</creatorcontrib><creatorcontrib>Pickup, Stephen</creatorcontrib><creatorcontrib>Choong, Soon Y</creatorcontrib><creatorcontrib>Li, Mingming</creatorcontrib><creatorcontrib>Xu, Hong</creatorcontrib><creatorcontrib>Gamble, Gregory D</creatorcontrib><creatorcontrib>Phillips, Anthony R J</creatorcontrib><creatorcontrib>Cowan, Brett R</creatorcontrib><creatorcontrib>Young, Alistair A</creatorcontrib><creatorcontrib>Cooper, Garth J S</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 Central (Corporate)</collection><collection>Immunology Abstracts</collection><collection>Health Medical collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</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)</collection><collection>ProQuest Central</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Publicly Available Content Database</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 China</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Cardiovascular diabetology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lu, Jun</au><au>Pontré, Beau</au><au>Pickup, Stephen</au><au>Choong, Soon Y</au><au>Li, Mingming</au><au>Xu, Hong</au><au>Gamble, Gregory D</au><au>Phillips, Anthony R J</au><au>Cowan, Brett R</au><au>Young, Alistair A</au><au>Cooper, Garth J S</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Treatment with a copper-selective chelator causes substantive improvement in cardiac function of diabetic rats with left-ventricular impairment</atitle><jtitle>Cardiovascular diabetology</jtitle><addtitle>Cardiovasc Diabetol</addtitle><date>2013-01-31</date><risdate>2013</risdate><volume>12</volume><issue>1</issue><spage>28</spage><epage>28</epage><pages>28-28</pages><artnum>28</artnum><issn>1475-2840</issn><eissn>1475-2840</eissn><abstract><![CDATA[Defective copper regulation is implicated as a causative mechanism of organ damage in diabetes. Treatment with trientine, a divalent-copper-selective chelator, improves arterial and renal structure/function in diabetes, wherein it also ameliorates left-ventricular (LV) hypertrophy. However, direct in vivo evidence that trientine can improve cardiac function in heart failure has hitherto been lacking.
To determine whether trientine treatment could improve in vivo outcome, we measured cardiac function in groups of trientine-treated diabetic (TETA-DIA), non-drug-treated diabetic (DIA) and sham-treated control (SHAM) rats, by using in vivo high-field cardiac magnetic-resonance imaging (cMRI) and an ex vivo isolated-perfused working heart method. Forty age-matched animals underwent a cMRI scan after which 12 were randomized to the SHAM group and 28 underwent streptozotocin-injection; of these, 25 developed stable diabetes, and 12 were then randomized to receive no treatment for 16 weeks (DIA) and the other 13 to undergo 8-weeks' untreated diabetes followed by 8-weeks' drug treatment (TETA-DIA). Animals were studied again by cMRI at 8 and 16 weeks following disease induction, and finally by measurement of ex vivo cardiac function.
After eight weeks diabetes, rats (DIA/TETA-DIA) had developed significant impairment of LV function, as judged by impairment of ejection fraction (LVEF), cardiac output (CO), and LV mass (LVM)/body-mass (all P < 0.001), as well as other functional indexes. LVEF, CO (both P < 0.001) and the other indexes deteriorated further at 16 weeks in DIA, whereas trientine (TETA-DIA) improved cardiac function by elevating LVEF and CO (both P < 0.001), and also partially reversed the increase in LVM/body-mass (P < 0.05). In ex vivo hearts from DIA, the CO response to increasing preload pressure was deficient compared with SHAM (P < 0.001) whereas the preload-CO relationship was significantly improved in TETA-DIA animals (P < 0.001).
Trientine treatment significantly improved cardiac function in diabetic rats with substantive LV impairment. These results implicate impaired copper regulation in the pathogenesis of impaired cardiac function caused by diabetic cardiomyopathy, and support ongoing studies of trientine treatment in patients with heart failure.]]></abstract><cop>England</cop><pub>BioMed Central</pub><pmid>23368770</pmid><doi>10.1186/1475-2840-12-28</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Cardiovascular diabetology, 2013-01, Vol.12 (1), p.28-28, Article 28 |
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| source | Publicly Available Content Database; PubMed Central |
| subjects | Animals Chelating Agents - pharmacology Chelating Agents - therapeutic use Copper Diabetes Diabetes Mellitus, Experimental - drug therapy Diabetes Mellitus, Experimental - physiopathology Heart - drug effects Heart - physiology Heart failure Heart Function Tests Male Medical research Metabolic disorders Original Investigation Rats Rats, Wistar Rodents Treatment Outcome Trientine - pharmacology Trientine - therapeutic use Ventricular Dysfunction, Left - drug therapy Ventricular Dysfunction, Left - physiopathology |
| title | Treatment with a copper-selective chelator causes substantive improvement in cardiac function of diabetic rats with left-ventricular impairment |
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