{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,7]],"date-time":"2026-10-07T23:17:38Z","timestamp":1791415058070,"version":"4.3.3"},"reference-count":42,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"1","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["Circulation Research"],"published-print":{"date-parts":[[2013,1,4]]},"abstract":"<jats:sec>\n            <jats:title>\n              <jats:underline>Rationale:<\/jats:underline>\n            <\/jats:title>\n            <jats:p>Muscle carnitine palmitoyltransferase I is predominant in the heart, but the liver isoform (liver carnitine palmitoyltransferase I [L-CPT1]) is elevated in hearts with low long chain fatty acid oxidation, such as fetal and hypertrophied hearts.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>\n              <jats:underline>Objective:<\/jats:underline>\n            <\/jats:title>\n            <jats:p>This work examined the effect of acute L-CPT1 expression on the regulation of palmitate oxidation and energy metabolism in intact functioning rat hearts for comparison with findings in hypertrophied hearts.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>\n              <jats:underline>Methods and Results:<\/jats:underline>\n            <\/jats:title>\n            <jats:p>\n              L-CPT1 was expressed in vivo in rat hearts by coronary perfusion of Adv.cmv.L-CPT1 (L-CPT1, n=15) vs phosphate-buffered saline (PBS) infusion (PBS, n=7) or empty virus (empty, n=5). L-CPT1 was elevated 5-fold at 72 hours after Adv.cmv.L-CPT1 infusion (\n              <jats:italic>P<\/jats:italic>\n              &lt;0.05), but muscle carnitine palmitoyltransferase I was unaffected. Despite similar tricarboxylic acid cycle rates, palmitate oxidation rates were reduced with L-CPT1 (1.12 \u00b1 0.29 \u03bcmol\/min per gram of dry weight, mean\u00b1SE) vs PBS (1.6 \u00b1 0.34). Acetyl CoA production from palmitate was reduced with L-CPT1 (69 \u00b1 0.02%;\n              <jats:italic>P<\/jats:italic>\n              &lt;0.05; PBS=79 \u00b1 0.01%; empty=81 \u00b1 0.02%), similar to what occurs in hypertrophied hearts, and with no difference in malonyl CoA content. Glucose oxidation was elevated with L-CPT1 (by 60%). Surprisingly, L-CPT1 hearts contained elevated atrial natriuretic peptide, indicating induction of hypertrophic signaling.\n            <\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>\n              <jats:underline>Conclusions:<\/jats:underline>\n            <\/jats:title>\n            <jats:p>The results link L-CPT1 expression to reduced palmitate oxidation in a nondiseased adult heart, recapitulating the phenotype of reduced long chain fatty acid oxidation in cardiac hypertrophy. The implications are that L-CPT1 expression induces metabolic remodeling hypertrophic signaling and that regulatory factors beyond malonyl CoA in the heart regulate long chain fatty acid oxidation via L-CPT1.<\/jats:p>\n          <\/jats:sec>","DOI":"10.1161\/circresaha.112.274456","type":"journal-article","created":{"date-parts":[[2012,9,15]],"date-time":"2012-09-15T11:31:58Z","timestamp":1347708718000},"page":"57-65","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":35,"title":["Acute Liver Carnitine Palmitoyltransferase I Overexpression Recapitulates Reduced Palmitate Oxidation of Cardiac Hypertrophy"],"prefix":"10.1161","volume":"112","author":[{"given":"E. Douglas","family":"Lewandowski","sequence":"first","affiliation":[{"name":"From the Center for Cardiovascular Research, University of Illinois at Chicago College of Medicine, Chicago, IL (E.D.L., S.K.F., M.F., N.H.B., X.W., J.M.O.); Division of Cardiology, Department of Medicine, University of Colorado School of Medicine, Aurora, CO (L.A.W.); and Mazankowski Alberta Heart Institute, Departments of Pediatrics and Pharmacology, University of Alberta, Edmonton, Alberta, Canada (A.H., G.D.L.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Susan K.","family":"Fischer","sequence":"additional","affiliation":[{"name":"From the Center for Cardiovascular Research, University of Illinois at Chicago College of Medicine, Chicago, IL (E.D.L., S.K.F., M.F., N.H.B., X.W., J.M.O.); Division of Cardiology, Department of Medicine, University of Colorado School of Medicine, Aurora, CO (L.A.W.); and Mazankowski Alberta Heart Institute, Departments of Pediatrics and Pharmacology, University of Alberta, Edmonton, Alberta, Canada (A.H., G.D.L.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Matthew","family":"Fasano","sequence":"additional","affiliation":[{"name":"From the Center for Cardiovascular Research, University of Illinois at Chicago College of Medicine, Chicago, IL (E.D.L., S.K.F., M.F., N.H.B., X.W., J.M.O.); Division of Cardiology, Department of Medicine, University of Colorado School of Medicine, Aurora, CO (L.A.W.); and Mazankowski Alberta Heart Institute, Departments of Pediatrics and Pharmacology, University of Alberta, Edmonton, Alberta, Canada (A.H., G.D.L.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Natasha H.","family":"Banke","sequence":"additional","affiliation":[{"name":"From the Center for Cardiovascular Research, University of Illinois at Chicago College of Medicine, Chicago, IL (E.D.L., S.K.F., M.F., N.H.B., X.W., J.M.O.); Division of Cardiology, Department of Medicine, University of Colorado School of Medicine, Aurora, CO (L.A.W.); and Mazankowski Alberta Heart Institute, Departments of Pediatrics and Pharmacology, University of Alberta, Edmonton, Alberta, Canada (A.H., G.D.L.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lori A.","family":"Walker","sequence":"additional","affiliation":[{"name":"From the Center for Cardiovascular Research, University of Illinois at Chicago College of Medicine, Chicago, IL (E.D.L., S.K.F., M.F., N.H.B., X.W., J.M.O.); Division of Cardiology, Department of Medicine, University of Colorado School of Medicine, Aurora, CO (L.A.W.); and Mazankowski Alberta Heart Institute, Departments of Pediatrics and Pharmacology, University of Alberta, Edmonton, Alberta, Canada (A.H., G.D.L.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Alda","family":"Huqi","sequence":"additional","affiliation":[{"name":"From the Center for Cardiovascular Research, University of Illinois at Chicago College of Medicine, Chicago, IL (E.D.L., S.K.F., M.F., N.H.B., X.W., J.M.O.); Division of Cardiology, Department of Medicine, University of Colorado School of Medicine, Aurora, CO (L.A.W.); and Mazankowski Alberta Heart Institute, Departments of Pediatrics and Pharmacology, University of Alberta, Edmonton, Alberta, Canada (A.H., G.D.L.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xuerong","family":"Wang","sequence":"additional","affiliation":[{"name":"From the Center for Cardiovascular Research, University of Illinois at Chicago College of Medicine, Chicago, IL (E.D.L., S.K.F., M.F., N.H.B., X.W., J.M.O.); Division of Cardiology, Department of Medicine, University of Colorado School of Medicine, Aurora, CO (L.A.W.); and Mazankowski Alberta Heart Institute, Departments of Pediatrics and Pharmacology, University of Alberta, Edmonton, Alberta, Canada (A.H., G.D.L.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gary D.","family":"Lopaschuk","sequence":"additional","affiliation":[{"name":"From the Center for Cardiovascular Research, University of Illinois at Chicago College of Medicine, Chicago, IL (E.D.L., S.K.F., M.F., N.H.B., X.W., J.M.O.); Division of Cardiology, Department of Medicine, University of Colorado School of Medicine, Aurora, CO (L.A.W.); and Mazankowski Alberta Heart Institute, Departments of Pediatrics and Pharmacology, University of Alberta, Edmonton, Alberta, Canada (A.H., G.D.L.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"J. 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