Cause Cardiac Dysfunction in Diet-Induced Obesity Increased Glucose Uptake and Oxidation in Mouse Hearts Prevent High Fatty Acid

Oxidation but Cause Cardiac Dysfunction in Diet-Induced Obesity Increased Glucose Uptake and Oxidation in Mouse Hearts Prevent High Fatty Acid Print ISSN: 0009-7322. Online ISSN: 1524-4539 Copyright © 2009 American Heart Association, Inc. All rights reserved. is published by the American Heart Association, 7272 Greenville Avenue, Dallas, TX 75231 Circulation doi: 10.1161/CIRCULATIONAHA.108.832915 2009;119:2818-2828; originally published online May 18, 2009; Circulation. http://circ.ahajournals.org/content/119/21/2818 World Wide Web at: The online version of this article, along with updated information and services, is located on the http://circ.ahajournals.org/content/suppl/2009/05/18/CIRCULATIONAHA.108.832915.DC1.html Data Supplement (unedited) at:

[1]  Richard T. Lee,et al.  Targeted Deletion of Thioredoxin-Interacting Protein Regulates Cardiac Dysfunction in Response to Pressure Overload , 2007, Circulation research.

[2]  Mohit M. Jain,et al.  Long-Term Effects of Increased Glucose Entry on Mouse Hearts During Normal Aging and Ischemic Stress , 2007, Circulation.

[3]  E. Abel,et al.  Diabetic cardiomyopathy revisited. , 2007, Circulation.

[4]  P. D. de Tombe,et al.  p38-MAPK Induced Dephosphorylation of &agr;-Tropomyosin Is Associated With Depression of Myocardial Sarcomeric Tension and ATPase Activity , 2007, Circulation research.

[5]  B. Finck,et al.  The PPAR regulatory system in cardiac physiology and disease. , 2007, Cardiovascular research.

[6]  P. Ernsberger,et al.  CARNITINE PALMITOYL TRANSFERASE‐I INHIBITION IS NOT ASSOCIATED WITH CARDIAC HYPERTROPHY IN RATS FED A HIGH‐FAT DIET , 2007, Clinical and experimental pharmacology & physiology.

[7]  D. Kwiatkowski,et al.  Requirement of Rac1 in the development of cardiac hypertrophy. , 2006, Proceedings of the National Academy of Sciences of the United States of America.

[8]  J. Balschi,et al.  Decreased Contractile and Metabolic Reserve in Peroxisome Proliferator–Activated Receptor-&agr;–Null Hearts Can Be Rescued by Increasing Glucose Transport and Utilization , 2005, Circulation.

[9]  William C Stanley,et al.  Myocardial substrate metabolism in the normal and failing heart. , 2005, Physiological reviews.

[10]  Michael D. Schneider,et al.  Cardiomyocyte-restricted peroxisome proliferator-activated receptor-δ deletion perturbs myocardial fatty acid oxidation and leads to cardiomyopathy , 2004, Nature Medicine.

[11]  R. Tian Transcriptional regulation of energy substrate metabolism in normal and hypertrophied heart , 2003, Current hypertension reports.

[12]  Lionel H. Opie,et al.  Heart Physiology: From Cell to Circulation , 2003 .

[13]  Mohit M. Jain,et al.  Cardiac-Specific Overexpression of GLUT1 Prevents the Development of Heart Failure Attributable to Pressure Overload in Mice , 2002, Circulation.

[14]  N. Chandel,et al.  Mitochondrial ROS initiate phosphorylation of p38 MAP kinase during hypoxia in cardiomyocytes. , 2002, American journal of physiology. Lung cellular and molecular physiology.

[15]  D. Belke,et al.  Overexpression of the sarcoplasmic reticulum Ca(2+)-ATPase improves myocardial contractility in diabetic cardiomyopathy. , 2002, Diabetes.

[16]  Heping Cheng,et al.  Cellular Mechanisms of p 38 MAPK – Induced Negative Inotropic Effect : Suppression of Myofilament Ca , 2002 .

[17]  Thomas D. Schmittgen,et al.  Real-Time Quantitative PCR , 2002 .

[18]  G. Shipley,et al.  Uncoupling protein 3 transcription is regulated by peroxisome proliferator‐activated receptor α in the adult rodent heart , 2001, FASEB journal : official publication of the Federation of American Societies for Experimental Biology.

[19]  H. Taegtmeyer,et al.  Regulation of Energy Metabolism of the Heart during Acute Increase in Heart Work* , 1998, The Journal of Biological Chemistry.

[20]  A. Clerk,et al.  Stimulation of “Stress-regulated” Mitogen-activated Protein Kinases (Stress-activated Protein Kinases/c-Jun N-terminal Kinases and p38-Mitogen-activated Protein Kinases) in Perfused Rat Hearts by Oxidative and Other Stresses* , 1998, The Journal of Biological Chemistry.

[21]  G. Lopaschuk,et al.  Contribution of oxidative metabolism and glycolysis to ATP production in hypertrophied hearts. , 1994, The American journal of physiology.

[22]  G. Lopaschuk,et al.  Glycolysis is predominant source of myocardial ATP production immediately after birth. , 1991, The American journal of physiology.

[23]  A. Sherry,et al.  Analysis of tricarboxylic acid cycle of the heart using 13C isotope isomers. , 1990, The American journal of physiology.

[24]  R. Hajjar,et al.  Angiotensin II-induced negative inotropy in rat ventricular myocytes: role of reactive oxygen species and p38 MAPK. , 2006, American journal of physiology. Heart and circulatory physiology.

[25]  R. Liao,et al.  Galpha(i2) but not Galpha(i3) is required for muscarinic inhibition of contractility and calcium currents in adult cardiomyocytes. , 2000, Circulation research.

[26]  L. Opie Metabolism of the heart in health and disease. I. , 1968, American heart journal.