The Antianginal Drug Trimetazidine Shifts Cardiac Energy Metabolism From Fatty Acid Oxidation to Glucose Oxidation by Inhibiting Mitochondrial Long-Chain 3-Ketoacyl Coenzyme A Thiolase
ABSTRACTTrimetazidine is a clinically effective antianginal agent that has no negative inotropic or vasodilator properties. Although it is thought to have direct cytoprotective actions on the myocardium, the mechanism(s) by which this occurs is as yet undefined. In this study, we determined what eff...
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| Veröffentlicht in: | Circulation research 2000-03, Vol.86 (5), p.580-588 |
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| creator | Kantor, Paul F Lucien, Arnaud Kozak, Raymond Lopaschuk, Gary D |
| description | ABSTRACTTrimetazidine is a clinically effective antianginal agent that has no negative inotropic or vasodilator properties. Although it is thought to have direct cytoprotective actions on the myocardium, the mechanism(s) by which this occurs is as yet undefined. In this study, we determined what effects trimetazidine has on both fatty acid and glucose metabolism in isolated working rat hearts and on the activities of various enzymes involved in fatty acid oxidation. Hearts were perfused with Krebs-Henseleit solution containing 100 μU/mL insulin, 3% albumin, 5 mmol/L glucose, and fatty acids of different chain lengths. Both glucose and fatty acids were appropriately radiolabeled with either H or C for measurement of glycolysis, glucose oxidation, and fatty acid oxidation. Trimetazidine had no effect on myocardial oxygen consumption or cardiac work under any aerobic perfusion condition used. In hearts perfused with 5 mmol/L glucose and 0.4 mmol/L palmitate, trimetazidine decreased the rate of palmitate oxidation from 488±24 to 408±15 nmol · g dry weight · minute (P |
| doi_str_mv | 10.1161/01.res.86.5.580 |
| format | Article |
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Although it is thought to have direct cytoprotective actions on the myocardium, the mechanism(s) by which this occurs is as yet undefined. In this study, we determined what effects trimetazidine has on both fatty acid and glucose metabolism in isolated working rat hearts and on the activities of various enzymes involved in fatty acid oxidation. Hearts were perfused with Krebs-Henseleit solution containing 100 μU/mL insulin, 3% albumin, 5 mmol/L glucose, and fatty acids of different chain lengths. Both glucose and fatty acids were appropriately radiolabeled with either H or C for measurement of glycolysis, glucose oxidation, and fatty acid oxidation. Trimetazidine had no effect on myocardial oxygen consumption or cardiac work under any aerobic perfusion condition used. In hearts perfused with 5 mmol/L glucose and 0.4 mmol/L palmitate, trimetazidine decreased the rate of palmitate oxidation from 488±24 to 408±15 nmol · g dry weight · minute (P <0.05), whereas it increased rates of glucose oxidation from 1889±119 to 2378±166 nmol · g dry weight · minute (P <0.05). In hearts subjected to low-flow ischemia, trimetazidine resulted in a 210% increase in glucose oxidation rates. In both aerobic and ischemic hearts, glycolytic rates were unaltered by trimetazidine. The effects of trimetazidine on glucose oxidation were accompanied by a 37% increase in the active form of pyruvate dehydrogenase, the rate-limiting enzyme for glucose oxidation. No effect of trimetazidine was observed on glycolysis, glucose oxidation, fatty acid oxidation, or active pyruvate dehydrogenase when palmitate was substituted with 0.8 mmol/L octanoate or 1.6 mmol/L butyrate, suggesting that trimetazidine directly inhibits long-chain fatty acid oxidation. This reduction in fatty acid oxidation was accompanied by a significant decrease in the activity of the long-chain isoform of the last enzyme involved in fatty acid β-oxidation, 3-ketoacyl coenzyme A (CoA) thiolase activity (IC50 of 75 nmol/L). In contrast, concentrations of trimetazidine in excess of 10 and 100 μmol/L were needed to inhibit the medium- and short-chain forms of 3-ketoacyl CoA thiolase, respectively. Previous studies have shown that inhibition of fatty acid oxidation and stimulation of glucose oxidation can protect the ischemic heart. Therefore, our data suggest that the antianginal effects of trimetazidine may occur because of an inhibition of long-chain 3-ketoacyl CoA thiolase activity, which results in a reduction in fatty acid oxidation and a stimulation of glucose oxidation.</description><identifier>ISSN: 0009-7330</identifier><identifier>EISSN: 1524-4571</identifier><identifier>DOI: 10.1161/01.res.86.5.580</identifier><identifier>PMID: 10720420</identifier><identifier>CODEN: CIRUAL</identifier><language>eng</language><publisher>Hagerstown, MD: American Heart Association, Inc</publisher><subject>Angina Pectoris - drug therapy ; Angina Pectoris - metabolism ; Animals ; Antianginal agents. Coronary vasodilator agents ; Biological and medical sciences ; Carboxy-Lyases - metabolism ; Cardiovascular system ; Dose-Response Relationship, Drug ; Energy Metabolism - drug effects ; Esters - metabolism ; Fatty Acids - metabolism ; Fatty Acids - pharmacology ; Glucose - metabolism ; Glycolysis - drug effects ; Male ; Malonyl Coenzyme A - metabolism ; Medical sciences ; Mitochondria - drug effects ; Mitochondria - metabolism ; Mitochondrial Trifunctional Protein ; Multienzyme Complexes - metabolism ; Myocardial Ischemia - drug therapy ; Myocardial Ischemia - metabolism ; Myocardium - enzymology ; Pharmacology. Drug treatments ; Pyruvate Dehydrogenase Complex - metabolism ; Rats ; Rats, Sprague-Dawley ; Trimetazidine - pharmacology ; Vasodilator Agents - pharmacology</subject><ispartof>Circulation research, 2000-03, Vol.86 (5), p.580-588</ispartof><rights>2000 American Heart Association, Inc.</rights><rights>2000 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5565-39dbf1f1df2055d16efbc88b9ad44fd23881ee2e54ef90a5c65d3913fc838ab03</citedby><cites>FETCH-LOGICAL-c5565-39dbf1f1df2055d16efbc88b9ad44fd23881ee2e54ef90a5c65d3913fc838ab03</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,3687,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=1317578$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/10720420$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kantor, Paul F</creatorcontrib><creatorcontrib>Lucien, Arnaud</creatorcontrib><creatorcontrib>Kozak, Raymond</creatorcontrib><creatorcontrib>Lopaschuk, Gary D</creatorcontrib><title>The Antianginal Drug Trimetazidine Shifts Cardiac Energy Metabolism From Fatty Acid Oxidation to Glucose Oxidation by Inhibiting Mitochondrial Long-Chain 3-Ketoacyl Coenzyme A Thiolase</title><title>Circulation research</title><addtitle>Circ Res</addtitle><description>ABSTRACTTrimetazidine is a clinically effective antianginal agent that has no negative inotropic or vasodilator properties. Although it is thought to have direct cytoprotective actions on the myocardium, the mechanism(s) by which this occurs is as yet undefined. In this study, we determined what effects trimetazidine has on both fatty acid and glucose metabolism in isolated working rat hearts and on the activities of various enzymes involved in fatty acid oxidation. Hearts were perfused with Krebs-Henseleit solution containing 100 μU/mL insulin, 3% albumin, 5 mmol/L glucose, and fatty acids of different chain lengths. Both glucose and fatty acids were appropriately radiolabeled with either H or C for measurement of glycolysis, glucose oxidation, and fatty acid oxidation. Trimetazidine had no effect on myocardial oxygen consumption or cardiac work under any aerobic perfusion condition used. In hearts perfused with 5 mmol/L glucose and 0.4 mmol/L palmitate, trimetazidine decreased the rate of palmitate oxidation from 488±24 to 408±15 nmol · g dry weight · minute (P <0.05), whereas it increased rates of glucose oxidation from 1889±119 to 2378±166 nmol · g dry weight · minute (P <0.05). In hearts subjected to low-flow ischemia, trimetazidine resulted in a 210% increase in glucose oxidation rates. In both aerobic and ischemic hearts, glycolytic rates were unaltered by trimetazidine. The effects of trimetazidine on glucose oxidation were accompanied by a 37% increase in the active form of pyruvate dehydrogenase, the rate-limiting enzyme for glucose oxidation. No effect of trimetazidine was observed on glycolysis, glucose oxidation, fatty acid oxidation, or active pyruvate dehydrogenase when palmitate was substituted with 0.8 mmol/L octanoate or 1.6 mmol/L butyrate, suggesting that trimetazidine directly inhibits long-chain fatty acid oxidation. This reduction in fatty acid oxidation was accompanied by a significant decrease in the activity of the long-chain isoform of the last enzyme involved in fatty acid β-oxidation, 3-ketoacyl coenzyme A (CoA) thiolase activity (IC50 of 75 nmol/L). In contrast, concentrations of trimetazidine in excess of 10 and 100 μmol/L were needed to inhibit the medium- and short-chain forms of 3-ketoacyl CoA thiolase, respectively. Previous studies have shown that inhibition of fatty acid oxidation and stimulation of glucose oxidation can protect the ischemic heart. Therefore, our data suggest that the antianginal effects of trimetazidine may occur because of an inhibition of long-chain 3-ketoacyl CoA thiolase activity, which results in a reduction in fatty acid oxidation and a stimulation of glucose oxidation.</description><subject>Angina Pectoris - drug therapy</subject><subject>Angina Pectoris - metabolism</subject><subject>Animals</subject><subject>Antianginal agents. Coronary vasodilator agents</subject><subject>Biological and medical sciences</subject><subject>Carboxy-Lyases - metabolism</subject><subject>Cardiovascular system</subject><subject>Dose-Response Relationship, Drug</subject><subject>Energy Metabolism - drug effects</subject><subject>Esters - metabolism</subject><subject>Fatty Acids - metabolism</subject><subject>Fatty Acids - pharmacology</subject><subject>Glucose - metabolism</subject><subject>Glycolysis - drug effects</subject><subject>Male</subject><subject>Malonyl Coenzyme A - metabolism</subject><subject>Medical sciences</subject><subject>Mitochondria - drug effects</subject><subject>Mitochondria - metabolism</subject><subject>Mitochondrial Trifunctional Protein</subject><subject>Multienzyme Complexes - metabolism</subject><subject>Myocardial Ischemia - drug therapy</subject><subject>Myocardial Ischemia - metabolism</subject><subject>Myocardium - enzymology</subject><subject>Pharmacology. Drug treatments</subject><subject>Pyruvate Dehydrogenase Complex - metabolism</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Trimetazidine - pharmacology</subject><subject>Vasodilator Agents - pharmacology</subject><issn>0009-7330</issn><issn>1524-4571</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2000</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpN0k1vFCEYB_CJ0di1evZmOBhvs-VlmJfjZrutjds0seuZMPDMDspCBSZ1-sn8eKK7ib3wEPLjgfCnKN4TvCSkJheYLAPEZVsv-ZK3-EWxIJxWZcUb8rJYYIy7smEMnxVvYvyOMakY7V4XZwQ3FFcUL4rfuxHQyiUj3d44adFlmPZoF8wBknwy2jhA96MZUkRrGbSRCm0chP2MbjPovTXxgK6Cz4NMaUYrZTS6-2W0TMY7lDy6tpPyEZ4t9jO6caPpTTJuj25N8mr0TgeTj996ty_XozQOsfILJC_VbNHag3uaD_mmaDcab2WEt8WrQdoI7071vPh2tdmtP5fbu-ub9WpbKs5rXrJO9wMZiB4o5lyTGoZetW3fSV1Vg6asbQkABV7B0GHJVc016wgbVMta2WN2Xnw69n0I_ucEMYmDiQqslQ78FEWDu4byhmZ4cYQq-BgDDOIhv6IMsyBY_A1LYCK-bu5FWwsuclh5x4dT66k_gH7mj-lk8PEEZFTSDkE6ZeJ_x0jDmzaz6sgevU0Q4g87PUIQI0ibRpE_AWaY0JL-m5EGl7kSzv4AV_evjA</recordid><startdate>20000317</startdate><enddate>20000317</enddate><creator>Kantor, Paul F</creator><creator>Lucien, Arnaud</creator><creator>Kozak, Raymond</creator><creator>Lopaschuk, Gary D</creator><general>American Heart Association, Inc</general><general>Lippincott</general><scope>IQODW</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>7X8</scope></search><sort><creationdate>20000317</creationdate><title>The Antianginal Drug Trimetazidine Shifts Cardiac Energy Metabolism From Fatty Acid Oxidation to Glucose Oxidation by Inhibiting Mitochondrial Long-Chain 3-Ketoacyl Coenzyme A Thiolase</title><author>Kantor, Paul F ; Lucien, Arnaud ; Kozak, Raymond ; Lopaschuk, Gary D</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5565-39dbf1f1df2055d16efbc88b9ad44fd23881ee2e54ef90a5c65d3913fc838ab03</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2000</creationdate><topic>Angina Pectoris - drug therapy</topic><topic>Angina Pectoris - metabolism</topic><topic>Animals</topic><topic>Antianginal agents. Coronary vasodilator agents</topic><topic>Biological and medical sciences</topic><topic>Carboxy-Lyases - metabolism</topic><topic>Cardiovascular system</topic><topic>Dose-Response Relationship, Drug</topic><topic>Energy Metabolism - drug effects</topic><topic>Esters - metabolism</topic><topic>Fatty Acids - metabolism</topic><topic>Fatty Acids - pharmacology</topic><topic>Glucose - metabolism</topic><topic>Glycolysis - drug effects</topic><topic>Male</topic><topic>Malonyl Coenzyme A - metabolism</topic><topic>Medical sciences</topic><topic>Mitochondria - drug effects</topic><topic>Mitochondria - metabolism</topic><topic>Mitochondrial Trifunctional Protein</topic><topic>Multienzyme Complexes - metabolism</topic><topic>Myocardial Ischemia - drug therapy</topic><topic>Myocardial Ischemia - metabolism</topic><topic>Myocardium - enzymology</topic><topic>Pharmacology. Drug treatments</topic><topic>Pyruvate Dehydrogenase Complex - metabolism</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Trimetazidine - pharmacology</topic><topic>Vasodilator Agents - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kantor, Paul F</creatorcontrib><creatorcontrib>Lucien, Arnaud</creatorcontrib><creatorcontrib>Kozak, Raymond</creatorcontrib><creatorcontrib>Lopaschuk, Gary D</creatorcontrib><collection>Pascal-Francis</collection><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>Circulation research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kantor, Paul F</au><au>Lucien, Arnaud</au><au>Kozak, Raymond</au><au>Lopaschuk, Gary D</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The Antianginal Drug Trimetazidine Shifts Cardiac Energy Metabolism From Fatty Acid Oxidation to Glucose Oxidation by Inhibiting Mitochondrial Long-Chain 3-Ketoacyl Coenzyme A Thiolase</atitle><jtitle>Circulation research</jtitle><addtitle>Circ Res</addtitle><date>2000-03-17</date><risdate>2000</risdate><volume>86</volume><issue>5</issue><spage>580</spage><epage>588</epage><pages>580-588</pages><issn>0009-7330</issn><eissn>1524-4571</eissn><coden>CIRUAL</coden><abstract>ABSTRACTTrimetazidine is a clinically effective antianginal agent that has no negative inotropic or vasodilator properties. Although it is thought to have direct cytoprotective actions on the myocardium, the mechanism(s) by which this occurs is as yet undefined. In this study, we determined what effects trimetazidine has on both fatty acid and glucose metabolism in isolated working rat hearts and on the activities of various enzymes involved in fatty acid oxidation. Hearts were perfused with Krebs-Henseleit solution containing 100 μU/mL insulin, 3% albumin, 5 mmol/L glucose, and fatty acids of different chain lengths. Both glucose and fatty acids were appropriately radiolabeled with either H or C for measurement of glycolysis, glucose oxidation, and fatty acid oxidation. Trimetazidine had no effect on myocardial oxygen consumption or cardiac work under any aerobic perfusion condition used. In hearts perfused with 5 mmol/L glucose and 0.4 mmol/L palmitate, trimetazidine decreased the rate of palmitate oxidation from 488±24 to 408±15 nmol · g dry weight · minute (P <0.05), whereas it increased rates of glucose oxidation from 1889±119 to 2378±166 nmol · g dry weight · minute (P <0.05). In hearts subjected to low-flow ischemia, trimetazidine resulted in a 210% increase in glucose oxidation rates. In both aerobic and ischemic hearts, glycolytic rates were unaltered by trimetazidine. The effects of trimetazidine on glucose oxidation were accompanied by a 37% increase in the active form of pyruvate dehydrogenase, the rate-limiting enzyme for glucose oxidation. No effect of trimetazidine was observed on glycolysis, glucose oxidation, fatty acid oxidation, or active pyruvate dehydrogenase when palmitate was substituted with 0.8 mmol/L octanoate or 1.6 mmol/L butyrate, suggesting that trimetazidine directly inhibits long-chain fatty acid oxidation. This reduction in fatty acid oxidation was accompanied by a significant decrease in the activity of the long-chain isoform of the last enzyme involved in fatty acid β-oxidation, 3-ketoacyl coenzyme A (CoA) thiolase activity (IC50 of 75 nmol/L). In contrast, concentrations of trimetazidine in excess of 10 and 100 μmol/L were needed to inhibit the medium- and short-chain forms of 3-ketoacyl CoA thiolase, respectively. Previous studies have shown that inhibition of fatty acid oxidation and stimulation of glucose oxidation can protect the ischemic heart. Therefore, our data suggest that the antianginal effects of trimetazidine may occur because of an inhibition of long-chain 3-ketoacyl CoA thiolase activity, which results in a reduction in fatty acid oxidation and a stimulation of glucose oxidation.</abstract><cop>Hagerstown, MD</cop><pub>American Heart Association, Inc</pub><pmid>10720420</pmid><doi>10.1161/01.res.86.5.580</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Circulation research, 2000-03, Vol.86 (5), p.580-588 |
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| subjects | Angina Pectoris - drug therapy Angina Pectoris - metabolism Animals Antianginal agents. Coronary vasodilator agents Biological and medical sciences Carboxy-Lyases - metabolism Cardiovascular system Dose-Response Relationship, Drug Energy Metabolism - drug effects Esters - metabolism Fatty Acids - metabolism Fatty Acids - pharmacology Glucose - metabolism Glycolysis - drug effects Male Malonyl Coenzyme A - metabolism Medical sciences Mitochondria - drug effects Mitochondria - metabolism Mitochondrial Trifunctional Protein Multienzyme Complexes - metabolism Myocardial Ischemia - drug therapy Myocardial Ischemia - metabolism Myocardium - enzymology Pharmacology. Drug treatments Pyruvate Dehydrogenase Complex - metabolism Rats Rats, Sprague-Dawley Trimetazidine - pharmacology Vasodilator Agents - pharmacology |
| title | The Antianginal Drug Trimetazidine Shifts Cardiac Energy Metabolism From Fatty Acid Oxidation to Glucose Oxidation by Inhibiting Mitochondrial Long-Chain 3-Ketoacyl Coenzyme A Thiolase |
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