Restoration of glucose metabolism in leptin-resistant mouse hearts after acute myocardial infarction through the activation of survival kinase pathways

Journal of Molecular and Cellular Cardiology

Volumn 53, Issue 1, 2012, Pages 91-100

  Witham, William ^a   Yester, Keith ^a   O'Donnell, Christopher P ^a   McGaffin, Kenneth R ^a  

^a UNIVERSITY OF PITTSBURGH MEDICAL CENTER   (United States)

Author keywords

Leptin; Metabolism; Myocardial infarction; Pyruvate dehydrogenase; Survival kinases

Indexed keywords

CILIARY NEUROTROPHIC FACTOR; CYTOCHROME C OXIDASE; LEPTIN; MULTIENZYME COMPLEX; PHOSPHATIDYLINOSITOL 3 KINASE; PROTEIN KINASE B; PYRUVATE DEHYDROGENASE; PYRUVATE DEHYDROGENASE KINASE; REDUCED NICOTINAMIDE ADENINE DINUCLEOTIDE DEHYDROGENASE (UBIQUINONE); STAT3 PROTEIN; SUCCINATE DEHYDROGENASE (UBIQUINONE); TAMOXIFEN; UBIQUINOL CYTOCHROME C REDUCTASE;

ACUTE HEART INFARCTION; ANIMAL CELL; ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; ARTICLE; CONTROLLED STUDY; ELECTRON TRANSPORT; ENZYME ACTIVATION; ENZYME ACTIVITY; FATTY ACID OXIDATION; GLUCOSE METABOLISM; GLUCOSE OXIDATION; GLUCOSE UTILIZATION; GLYCOLYSIS; HEART MUSCLE CELL; HEART STRESS; HOMOZYGOSITY; LIPID PEROXIDATION; MALE; MORBIDITY; MOUSE; NONHUMAN; OXIDATIVE PHOSPHORYLATION; OXIDATIVE STRESS; PRIORITY JOURNAL; PROTEIN EXPRESSION; PROTEIN PHOSPHORYLATION; SIGNAL TRANSDUCTION;

ANIMALS; CILIARY NEUROTROPHIC FACTOR; FATTY ACIDS; GLUCOSE; HEART; MALE; MICE; MICE, KNOCKOUT; MITOCHONDRIA; MYOCARDIAL INFARCTION; MYOCARDIUM; OXIDATION-REDUCTION; OXIDATIVE STRESS; RECEPTORS, LEPTIN; SIGNAL TRANSDUCTION; TAMOXIFEN;

MUS;

EID: 84861964228     PISSN: 00222828     EISSN: 10958584     Source Type: Journal    
DOI: 10.1016/j.yjmcc.2012.03.016     Document Type: Article

References (42)

1. Taegtmeyer H., Hems R., Krebs H.A. Utilization of energy-providing substrates in the isolated working rat heart. Biochem J 1980, 186:701-711.
2. Amorim P.A., Nguyen T.D., Shingu Y., Schwarzer M., Mohr F.W., Schrepper A., et al. Myocardial infarction in rats causes partial impairment in insulin response associated with reduced fatty acid oxidation and mitochondrial gene expression. J Thorac Cardiovasc Surg 2010, 140:1160-1167.
3. Hansen C.A., Fellenius E., Neely J.R. Metabolic rates in normal and infarcted myocardium. Can J Cardiol 1986, (Suppl. A):1A-8A.
4. Tuunanen H., Ukkonen H., Knuuti J. Myocardial fatty acid metabolism and cardiac performance in heart failure. Curr Cardiol Rep 2008, 10:142-148.
5. Remondino A., Rosenblatt-Velin N., Montessuit C., Tardy I., Papageorgiou I., Dorsaz P.A., et al. Altered expression of proteins of metabolic regulation during remodeling of the left ventricle after myocardial infarction. J Mol Cell Cardiol 2000, 32:2025-2034.
6. Nagoshi T., Yoshimura M., Rosano G.M., Lopaschuk G.D., Mochizuki S. Optimization of Cardiac Metabolism in Heart Failure. Curr Pharm Des 2011, 35:3846-3853.
7. Stanley W.C., Recchia F.A., Lopaschuk G.D. Myocardial substrate metabolism in the normal and failing heart. Physiol Rev 2005, 85:1093-1129.
8. Hwang Y.C., Bakr S., Ramasamy R., Bergmann S.R. Relative importance of enhanced glucose uptake versus attenuation of long-chain acyl carnitines in protecting ischemic myocardium. Coron Artery Dis 2002, 13:313-318.
9. Folmes C.D., Sowah D., Clanachan A.S., Lopaschuk G.D. High rates of residual fatty acid oxidation during mild ischemia decrease cardiac work and efficiency. J Mol Cell Cardiol 2009, 47:142-148.
10. Liu Q., Docherty J.C., Rendell J.C., Clanachan A.S., Lopaschuk G.D. High levels of fatty acids delay the recovery of intracellular pH and cardiac efficiency in post-ischemic hearts by inhibiting glucose oxidation. J Am Coll Cardiol 2002, 39:718-725.
11. Huang X.Q., Liedtke A.J. Alterations in fatty acid oxidation in ischemic and reperfused myocardium. Mol Cell Biochem 1989, 88:145-153.
12. Hausenloy D.J., Yellon D.M. Survival kinases in ischemic preconditioning and postconditioning. Cardiovasc Res 2006, 70:240-253.
13. Goodman M.D., Koch S.E., Fuller-Bicer G.A., Butler K.L. Regulating RISK: a role for JAK-STAT signaling in postconditioning?. Am J Physiol Heart Circ Physiol 2008, 295:H1649-H1656.
14. Smith C.C., Dixon R.A., Wynne A.M., Theodorou L., Ong S.G., Subrayan S., et al. Leptin-induced cardioprotection involves JAK/STAT signaling that may be linked to the mitochondrial permeability transition pore. Am J Physiol Heart Circ Physiol 2010, 299:H1265-H1270.
15. Abel E.D. Myocardial insulin resistance and cardiac complications of diabetes. Curr Drug Targets Immune Endocr Metabol Disord 2005, 5:219-226.
16. Lambert P.D., Anderson K.D., Sleeman M.W., Wong V., Tan J., Hijarunguru A., et al. Ciliary neurotrophic factor activates leptin-like pathways and reduces body fat, without cachexia or rebound weight gain, even in leptin-resistant obesity. Proc Natl Acad Sci U S A 2001, 98:4652-4657.
17. McGaffin K.R., Witham W.G., Yester K.A., Romano L.C., O'Doherty R.M., McTiernan C.F., et al. Cardiac-specific leptin receptor deletion exacerbates ischaemic heart failure in mice. Cardiovasc Res 2011, 89:60-71.
18. Belke D.D., Larsen T.S., Lopaschuk G.D., Severson D.L. Glucose and fatty acid metabolism in the isolated working mouse heart. Am J Physiol 1999, 277:R1210-R1217.
19. Buchanan J., Mazumder P.K., Hu P., Chakrabarti G., Roberts M.W., Yun U.J., et al. Reduced cardiac efficiency and altered substrate metabolism precedes the onset of hyperglycemia and contractile dysfunction in two mouse models of insulin resistance and obesity. Endocrinology 2005, 146:5341-5349.
20. Boudina S., Sena S., O'Neill B.T., Tathireddy P., Young M.E., Abel E.D. Reduced mitochondrial oxidative capacity and increased mitochondrial uncoupling impair myocardial energetics in obesity. Circulation 2005, 112:2686-2695.
21. Boudina S., Sena S., Theobald H., Sheng X., Wright J.J., Hu X.X., et al. Mitochondrial energetics in the heart in obesity-related diabetes: direct evidence for increased uncoupled respiration and activation of uncoupling proteins. Diabetes 2007, 56:2457-2466.
22. Opie L.H. The heart: physiology, from cell to circulation 1998, 295-342. Lippencott-Raven, New York. 3rd edition.
23. Ravichandran L.V., Chen H., Li Y., Quon M.J. Phosphorylation of PTP1B at Ser(50) by Akt impairs its ability to dephosphorylate the insulin receptor. Mol Endocrinol 2001, 15:1768-1780.
24. Keung W., Cadete V.J., Palaniyappan A., Jablonski A., Fischer M., Lopaschuk G.D. Intracerebroventricular leptin administration differentially alters cardiac energy metabolism in mice fed a low-fat and high-fat diet. J Cardiovasc Pharmacol 2011, 57:103-113.
25. Zhao Y.T., Weng C.L., Chen M.L., Li K.B., Ge Y.G., Lin X.M., et al. Comparison of glucose-insulin-potassium and insulin-glucose as adjunctive therapy in acute myocardial infarction: a contemporary meta-analysis of randomised controlled trials. Heart 2010, 96:1622-1626.
26. Lewandowski E.D., White L.T. Pyruvate dehydrogenase influences postischemic heart function. Circulation 1995, 91:2071-2079.
27. Ussher J.R., Lopaschuk G.D. The malonyl CoA axis as a potential target for treating ischaemic heart disease. Cardiovasc Res 2008, 79:259-268.
28. Burkart E.M., Sambandam N., Han X., Gross R.W., Courtois M., Gierasch C.M., et al. Nuclear receptors PPARbeta/delta and PPARalpha direct distinct metabolic regulatory programs in the mouse heart. J Clin Invest 2007, 117:3930-3939.
29. Madrazo J.A., Kelly D.P. The PPAR trio: regulators of myocardial energy metabolism in health and disease. J Mol Cell Cardiol 2008, 44:968-975.
30. Sloan C., Tuinei J., Nemetz K., Frandsen J., Soto J., Wride N., et al. Central leptin signaling is required to normalize myocardial fatty acid oxidation rates in caloric-restricted ob/ob mice. Diabetes 2011, 60:1424-1434.
31. McCormick J., Barry S.P., Sivarajah A., Stefanutti G., Townsend P.A., Lawrence K.M., et al. Free radical scavenging inhibits STAT phosphorylation following in vivo ischemia/reperfusion injury. FASEB J 2006, 20:2115-2117.
32. Hilfiker-Kleiner D., Hilfiker A., Drexler H. Many good reasons to have STAT3 in the heart. Pharmacol Ther 2005, 107:131-137.
33. Stephanou A. Role of STAT-1 and STAT-3 in ischaemia/reperfusion injury. J Cell Mol Med 2004, 8:519-525.
34. Wegrzyn J., Potla R., Chwae Y.J., Sepuri N.B., Zhang Q., Koeck T., et al. Function of mitochondrial Stat3 in cellular respiration. Science 2009, 323:793-797.
35. Heusch G., Musiolik J., Gedik N., Skyschally A. Mitochondrial STAT3 activation and cardioprotection by ischemic postconditioning in pigs with regional myocardial ischemia/reperfusion. Circ Res 2011, 109:1302-1308.
36. Liu Y., Fiskum G., Schubert D. Generation of reactive oxygen species by the mitochondrial electron transport chain. J Neurochem 2002, 80:780-787.
37. Stahl N., Yancopoulos G.D. The tripartite CNTF receptor complex: activation and signaling involves components shared with other cytokines. J Neurobiol 1994, 25:1454-1466.
38. Raju S.V., Zheng M., Schuleri K.H., Phan A.C., Bedja D., Saraiva R.M., et al. Activation of the cardiac ciliary neurotrophic factor receptor reverses left ventricular hypertrophy in leptin-deficient and leptin-resistant obesity. Proc Natl Acad Sci U S A 2006, 103:4222-4227.
39. Matthews V.B., Febbraio M.A. CNTF: a target therapeutic for obesity-related metabolic disease?. J Mol Med (Berl) 2008, 86:353-361.
40. Bongioanni P., Reali C., Sogos V. Ciliary neurotrophic factor (CNTF) for amyotrophic lateral sclerosis/motor neuron disease. Cochrane Database Syst Rev 2004, CD004302.
41. Ettinger M.P., Littlejohn T.W., Schwartz S.L., Weiss S.R., McIlwain H.H., Heymsfield S.B., et al. Recombinant variant of ciliary neurotrophic factor for weight loss in obese adults: a randomized, dose-ranging study. JAMA 2003, 289:1826-1832.
42. Flegal K.M., Carroll M.D., Ogden C.L., Curtin L.R. Prevalence and trends in obesity among US adults, 1999-2008. JAMA 2010, 303:235-241.