Optimization of cardiac metabolism in heart failure

Current Pharmaceutical Design

Volumn 17, Issue 35, 2011, Pages 3846-3853

  Nagoshi, Tomohisa ^a   Yoshimura, Michihiro ^a   Rosano, Giuseppe M C ^b   Lopaschuk, Gary D ^c   Mochizuki, Seibu ^a,d  

^a JIKEI UNIVERSITY SCHOOL OF MEDICINE   (Japan)

^b IRCCS SAN RAFFAELE PISANA   (Italy)

^c UNIVERSITY OF ALBERTA   (Canada)

^d MUSASHINO UNIVERSITY   (Japan)

Author keywords

Heart failure; Insulin resistance; Metabolic therapy; Myocardial glucose and fatty acid metabolism

Indexed keywords

ACETYL COENZYME A; ADENOSINE TRIPHOSPHATE; AMINO ACID; CARBOHYDRATE; CREATINE PHOSPHATE; DIPEPTIDYL PEPTIDASE IV INHIBITOR; DOBUTAMINE; ETOMOXIR; EXENDIN 4; FATTY ACID; GLUCAGON LIKE PEPTIDE 1; GLUCAGON LIKE PEPTIDE 1 DERIVATIVE; GLUCOSE; GLUCOSE TRANSPORTER; GLUCOSE TRANSPORTER 1; GLUCOSE TRANSPORTER 4; HYDROXYMETHYLGLUTARYL COENZYME A REDUCTASE KINASE; INSULIN; LACTIC ACID; LIRAGLUTIDE; OXFENICINE; PERHEXILINE; PHOSPHATIDYLINOSITOL 3 KINASE; PROTEIN KINASE B; PYRUVIC ACID; REDUCED NICOTINAMIDE ADENINE DINUCLEOTIDE; SITAGLIPTIN; SOMATOMEDIN C; TRIMETAZIDINE; UNINDEXED DRUG;

BLOOD SAMPLING; CELL GROWTH; CELL SURVIVAL; CITRIC ACID CYCLE; CORONARY ARTERY DISEASE; CYTOSOL; DRUG BLOOD LEVEL; DRUG EFFICACY; DRUG HALF LIFE; DRUG METABOLISM; DRUG SAFETY; ENERGY METABOLISM; ENZYME INHIBITION; ENZYME SYNTHESIS; FATTY ACID BLOOD LEVEL; FATTY ACID METABOLISM; FATTY ACID OXIDATION; GENE EXPRESSION; GLUCOSE BLOOD LEVEL; GLUCOSE METABOLISM; GLUCOSE OXIDATION; GLUCOSE TRANSPORT; GLYCOLYSIS; HEART; HEART CONTRACTION; HEART FAILURE; HEART LEFT VENTRICLE EJECTION FRACTION; HEART MUSCLE; HEART MUSCLE CELL; HEART MUSCLE ISCHEMIA; HEART MUSCLE METABOLISM; HEART PROTECTION; HUMAN; IN VITRO STUDY; IN VIVO STUDY; INSULIN BLOOD LEVEL; INSULIN RESISTANCE; LIVER TOXICITY; METABOLIC DISORDER; METABOLIC REGULATION; MORTALITY; OXIDATIVE STRESS; PHARMACOLOGIC STRESS TESTING; POSITRON EMISSION TOMOGRAPHY; PREVALENCE; PRIORITY JOURNAL; PROTEIN PHOSPHORYLATION; PROTEIN TRANSPORT; RECEPTOR UPREGULATION; RENIN ANGIOTENSIN ALDOSTERONE SYSTEM; REVIEW; SARCOLEMMA; SIGNAL TRANSDUCTION;

EID: 83455238338     PISSN: 13816128     EISSN: 18734286     Source Type: Journal    
DOI: 10.2174/138161211798357773     Document Type: Review

References (84)

1. Stanley WC, Recchia FA, Lopaschuk GD. Myocardial substrate metabolism in the normal and failing heart. Physiol Rev 2005; 85: 1093-1129.
2. Depre C, Vanoverschelde JL, Taegtmeyer H. Glucose for the heart. Circulation 1999; 99: 578-588.
3. Huss JM, Kelly DP. Mitochondrial energy metabolism in heart failure: a question of balance. J Clin Invest 2005; 115: 547-555.
4. Rosano GM, Fini M, Caminiti G, Barbaro G. Cardiac metabolism in myocardial ischemia. Curr Pharm Des 2008; 14: 2551-2562.
5. Mochizuki S, Neely JR. Control of glyceraldehyde-3-phosphate dehydrogenase in cardiac muscle. J Mol Cell Cardiol 1979; 11: 221-236.
6. Conway MA, Allis J, Ouwerkerk R, Niioka T, Rajagopalan B, Radda GK. Detection of low phosphocreatine to ATP ratio in failing hypertrophied human myocardium by 31P magnetic resonance spectroscopy. Lancet 1991; 338: 973-976.
7. Neubauer S, Horn M, Cramer M, et al. Myocardial phosphocreatine- to-ATP ratio is a predictor of mortality in patients with dilated cardiomyopathy. Circulation 1997; 96: 2190-2196.
8. Kantor PF, Lopaschuk GD, Opie LH. Myocardial Energy Metabolism. Heart Physiology and Pathophysiology 2001; Fourth edition: 543-69.
9. Witteles RM, Fowler MB. Insulin-resistant cardiomyopathy clinical evidence, mechanisms, and treatment options. J Am Coll Cardiol 2008; 51: 93-102.
10. Abozguia K, Shivu GN, Ahmed I, Phan TT, Frenneaux MP. The heart metabolism: pathophysiological aspects in ischaemia and heart failure. Curr Pharm Des 2009; 15: 827-835.
11. Paolisso G, Gambardella A, Galzerano D, et al. Total-body and myocardial substrate oxidation in congestive heart failure. Metabolism 1994; 43: 174-179.
12. Lommi J, Kupari M, Yki-Jarvinen H. Free fatty acid kinetics and oxidation in congestive heart failure. Am J Cardiol 1998; 81: 45-50.
13. Boudina S, Sena S, O'Neill BT, Tathireddy P, Young ME, Abel ED. Reduced mitochondrial oxidative capacity and increased mitochondrial uncoupling impair myocardial energetics in obesity. Circulation 2005; 112: 2686-2695.
14. Murray AJ, Anderson RE, Watson GC, Radda GK, Clarke K. Uncoupling proteins in human heart. Lancet 2004; 364: 1786-1788.
15. Murray AJ, Panagia M, Hauton D, Gibbons GF, Clarke K. Plasma free fatty acids and peroxisome proliferator-activated receptor alpha in the control of myocardial uncoupling protein levels. Diabetes 2005; 54: 3496-3402.
16. Xu KY, Zweier JL, Becker LC. Functional coupling between glycolysis and sarcoplasmic reticulum Ca2+ transport. Circ Res 1995; 77: 88-97.
17. Kusuoka H, Marban E. Mechanism of the diastolic dysfunction induced by glycolytic inhibition. Does adenosine triphosphate derived from glycolysis play a favored role in cellular Ca2+ homeostasis in ferret myocardium? J Clin Invest 1994; 93: 1216-1223.
18. Tani M. Mechanisms of Ca2+ overload in reperfused ischemic myocardium. Annu Rev Physiol 1990; 52: 543-559.
19. Vaughan-Jones RD, Spitzer KW, Swietach P. Intracellular pH regulation in heart. J Mol Cell Cardiol 2009; 46: 318-331.
20. Davila-Roman VG, Vedala G, Herrero P, et al. Altered myocardial fatty acid and glucose metabolism in idiopathic dilated cardiomyopathy. J Am Coll Cardiol 2002; 40: 271-277.
21. Chandler MP, Kerner J, Huang H, et al. Moderate severity heart failure does not involve a downregulation of myocardial fatty acid oxidation. Am J Physiol Heart Circ Physiol 2004; 287: H1538-H1543.
22. Osorio JC, Stanley WC, Linke A, et al. Impaired myocardial fatty acid oxidation and reduced protein expression of retinoid X receptor- alpha in pacing-induced heart failure. Circulation 2002; 106: 606-612.
23. Sack MN, Rader TA, Park S, Bastin J, McCune SA, Kelly DP. Fatty acid oxidation enzyme gene expression is downregulated in the failing heart. Circulation 1996; 94: 2837-2842.
24. Taylor M, Wallhaus TR, Degrado TR, et al. An evaluation of myocardial fatty acid and glucose uptake using PET with [18F]fluoro 6-thia-heptadecanoic acid and [18F]FDG in Patients with Congestive Heart Failure. J Nucl Med 2001; 42: 55-62.
25. Cook SA, Varela-Carver A, Mongillo M, et al. Abnormal myocardial insulin signalling in type 2 diabetes and left-ventricular dysfunction. Eur Heart J 2009.
26. Nikolaidis LA, Sturzu A, Stolarski C, Elahi D, Shen YT, Shannon RP. The development of myocardial insulin resistance in conscious dogs with advanced dilated cardiomyopathy. Cardiovasc Res 2004; 61: 297-306.
27. An D, Rodrigues B. Role of changes in cardiac metabolism in development of diabetic cardiomyopathy. Am J Physiol Heart Circ Physiol 2006; 291: H1489-H1506.
28. Lei B, Lionetti V, Young ME, et al. Paradoxical downregulation of the glucose oxidation pathway despite enhanced flux in severe heart failure. J Mol Cell Cardiol 2004; 36: 567-576.
29. O'Donnell JM, Fields AD, Sorokina N, Lewandowski ED. The absence of endogenous lipid oxidation in early stage heart failure exposes limits in lipid storage and turnover. J Mol Cell Cardiol 2008; 44: 315-322.
30. Melenovsky V, Benes J, Skaroupkova P, et al. Metabolic characterization of volume overload heart failure due to aorto-caval fistula in rats. Mol Cell Biochem 2011.
31. Sorokina N, O'Donnell JM, McKinney RD, et al. Recruitment of compensatory pathways to sustain oxidative flux with reduced carnitine palmitoyltransferase I activity characterizes inefficiency in energy metabolism in hypertrophied hearts. Circulation 2007; 115: 2033-2041.
32. Pound KM, Sorokina N, Ballal K, et al. Substrate-enzyme competition attenuates upregulated anaplerotic flux through malic enzyme in hypertrophied rat heart and restores triacylglyceride content: attenuating upregulated anaplerosis in hypertrophy. Circ Res 2009; 104: 805-812.
33. Winder WW. Energy-sensing and signaling by AMP-activated protein kinase in skeletal muscle. J Appl Physiol 2001; 91: 1017-1028.
34. Tian R, Musi N, D'Agostino J, Hirshman MF, Goodyear LJ. Increased adenosine monophosphate-activated protein kinase activity in rat hearts with pressure-overload hypertrophy. Circulation 2001; 104: 1664-1669.
35. Miller EJ, Li J, Leng L, et al. Macrophage migration inhibitory factor stimulates AMP-activated protein kinase in the ischaemic heart. Nature 2008; 451: 578-582.
36. Matsui T, Nagoshi T, Rosenzweig A. Akt and PI 3-Kinase Signaling in Cardiomyocyte Hypertrophy and Survival. Cell Cycle 2003; 2: 220-223.
37. Matsui T, Rosenzweig A. Convergent signal transduction pathways controlling cardiomyocyte survival and function: the role of PI 3- kinase and Akt. J Mol Cell Cardiol 2005; 38: 63-71.
38. Matsui T, Tao J, del Monte F, et al. Akt activation preserves cardiac function and prevents injury after transient cardiac ischemia in vivo. Circulation 2001; 104: 330-335.
39. Matsui T, Li L, Wu JC, et al. Phenotypic spectrum caused by transgenic overexpression of activated Akt in the heart. J Biol Chem 2002; 277: 22896-22901.
40. Matsui T, Nagoshi T, Hong EG, et al. Effects of chronic Akt activation on glucose uptake in the heart. Am J Physiol Endocrinol Metab 2006; 290: E789-E797.
41. Matsui T, Li L, del Monte F, et al. Adenoviral gene transfer of activated phosphatidylinositol 3'-kinase and Akt inhibits apoptosis of hypoxic cardiomyocytes in vitro. Circulation 1999; 100: 2373-2379.
42. Fujio Y, Nguyen T, Wencker D, Kitsis RN, Walsh K. Akt promotes survival of cardiomyocytes in vitro and protects against ischemiareperfusion injury in mouse heart. Circulation 2000; 101: 660-667.
43. Aikawa R, Nawano M, Gu Y, et al. Insulin prevents cardiomyocytes from oxidative stress-induced apoptosis through activation of PI3 kinase/Akt. Circulation 2000; 102: 2873-2879.
44. Yamashita K, Kajstura J, Discher DJ, et al. Reperfusion-activated Akt kinase prevents apoptosis in transgenic mouse hearts overexpressing insulin-like growth factor-1. Circ Res 2001; 88: 609-614.
45. Nagoshi T, Matsui T, Aoyama T, et al. PI3K rescues the detrimental effects of chronic Akt activation in the heart during ischemia/ reperfusion injury. J Clin Invest 2005; 115: 2128-2138.
46. Shiojima I, Sato K, Izumiya Y, et al. Disruption of coordinated cardiac hypertrophy and angiogenesis contributes to the transition to heart failure. J Clin Invest 2005; 115: 2108-2118.
47. Shimizu I, Minamino T, Toko H, et al. Excessive cardiac insulin signaling exacerbates systolic dysfunction induced by pressure overload in rodents. J Clin Invest 2010; 120: 1506-1514.
48. Lawlor MA, Alessi DR. PKB/Akt: a key mediator of cell proliferation, survival and insulin responses? J Cell Sci 2001; 114: 2903-2910.
49. Brazil DP, Hemmings BA. Ten years of protein kinase B signalling: a hard Akt to follow. Trends Biochem Sci 2001; 26: 657-664.
50. Haq S, Choukroun G, Lim H, et al. Differential activation of signal transduction pathways in human hearts with hypertrophy versus advanced heart failure. Circulation 2001; 103: 670-677.
51. Ananthakrishnan R, Moe GW, Goldenthal MJ, Marin-Garcia J. Akt signaling pathway in pacing-induced heart failure. Mol Cell Biochem 2005; 268: 103-110.
52. Yu Q, Gao F, Ma XL. Insulin says NO to cardiovascular disease. Cardiovasc Res 2011; 89: 516-524.
53. Schulz TJ, Westermann D, Isken F, et al. Activation of mitochondrial energy metabolism protects against cardiac failure. Aging (Albany NY) 2010; 2: 843-853.
54. Kim YK, Kim SJ, Yatani A, et al. Mechanism of enhanced cardiac function in mice with hypertrophy induced by overexpressed Akt. J Biol Chem 2003; 278: 47622-47628.
55. Kim SJ, Abdellatif M, Koul S, Crystal GJ. Chronic treatment with insulin-like growth factor I enhances myocyte contraction by upregulation of Akt-SERCA2a signaling pathway. Am J Physiol Heart Circ Physiol 2008; 295: H130-H135.
56. Catalucci D, Latronico MV, Ceci M, et al. Akt increases sarcoplasmic reticulum Ca2+ cycling by direct phosphorylation of phospholamban at Thr17. J Biol Chem 2009; 284: 28180-28187.
57. Hermann HP, Arp J, Pieske B, et al. Improved systolic and diastolic myocardial function with intracoronary pyruvate in patients with congestive heart failure. Eur J Heart Fail 2004; 6: 213-218.
58. Hasenfuss G, Maier LS, Hermann HP, et al. Influence of pyruvate on contractile performance and Ca(2+) cycling in isolated failing human myocardium. Circulation 2002; 105: 194-199.
59. Nikolaidis LA, Elahi D, Hentosz T, et al. Recombinant glucagonlike peptide-1 increases myocardial glucose uptake and improves left ventricular performance in conscious dogs with pacing-induced dilated cardiomyopathy. Circulation 2004; 110: 955-961.
60. Halbirk M, Norrelund H, Moller N, et al. Cardiovascular and metabolic effects of 48-h glucagon-like peptide-1 infusion in compensated chronic patients with heart failure. Am J Physiol Heart Circ Physiol 2010; 298: H1096-H1102.
61. Read PA, Khan FZ, Heck PM, Hoole SP, Dutka DP. DPP-4 inhibition by sitagliptin improves the myocardial response to dobutamine stress and mitigates stunning in a pilot study of patients with coronary artery disease. Circ Cardiovasc Imaging 2010; 3: 195-201.
62. Finck BN, Lehman JJ, Leone TC, et al. The cardiac phenotype induced by PPARalpha overexpression mimics that caused by diabetes mellitus. J Clin Invest 2002; 109: 121-130.
63. Yagyu H, Chen G, Yokoyama M, et al. Lipoprotein lipase (LpL) on the surface of cardiomyocytes increases lipid uptake and produces a cardiomyopathy. J Clin Invest 2003; 111: 419-426.
64. Kantor PF, Lucien A, Kozak R, Lopaschuk GD. The antianginal drug trimetazidine shifts cardiac energy metabolism from fatty acid oxidation to glucose oxidation by inhibiting mitochondrial longchain 3-ketoacyl coenzyme A thiolase. Circ Res 2000; 86: 580-588.
65. Vitale C, Wajngaten M, Sposato B, et al. Trimetazidine improves left ventricular function and quality of life in elderly patients with coronary artery disease. Eur Heart J 2004; 25: 1814-1821.
66. Fragasso G, Palloshi A, Puccetti P, et al. A randomized clinical trial of trimetazidine, a partial free fatty acid oxidation inhibitor, in patients with heart failure. J Am Coll Cardiol 2006; 48: 992-998.
67. Di Napoli P, Taccardi AA, Barsotti A. Long term cardioprotective action of trimetazidine and potential effect on the inflammatory process in patients with ischaemic dilated cardiomyopathy. Heart 2005; 91: 161-165.
68. Fragasso G, Perseghin G, De Cobelli F, et al. Effects of metabolic modulation by trimetazidine on left ventricular function and phosphocreatine/ adenosine triphosphate ratio in patients with heart failure. Eur Heart J 2006; 27: 942-948.
69. Zarain-Herzberg A, Rupp H, Elimban V, Dhalla NS. Modification of sarcoplasmic reticulum gene expression in pressure overload cardiac hypertrophy by etomoxir. FASEB J 1996; 10: 1303-1309.
70. Rupp H, Vetter R. Sarcoplasmic reticulum function and carnitine palmitoyltransferase-1 inhibition during progression of heart failure. Br J Pharmacol 2000; 131: 1748-1756.
71. Lee L, Campbell R, Scheuermann-Freestone M, et al. Metabolic modulation with perhexiline in chronic heart failure: a randomized, controlled trial of short-term use of a novel treatment. Circulation 2005; 112: 3280-3288.
72. Gilde AJ, van der Lee KA, Willemsen PH, et al. Peroxisome proliferator- activated receptor (PPAR) alpha and PPARbeta/delta, but not PPARgamma, modulate the expression of genes involved in cardiac lipid metabolism. Circ Res 2003; 92: 518-5124.
73. Kitamura K, Kangawa K, Matsuo H, Uyeda K. Phosphorylation of myocardial fructose-6-phosphate,2-kinase: fructose-2,6- bisphosphatase by cAMP-dependent protein kinase and protein kinase C. Activation by phosphorylation and amino acid sequences of the phosphorylation sites. J Biol Chem 1988; 263: 16796-16801.
74. Morisco C, Condorelli G, Trimarco V, et al. Akt mediates the cross-talk between beta-adrenergic and insulin receptors in neonatal cardiomyocytes. Circ Res 2005; 96: 180-188.
75. Wallhaus TR, Taylor M, DeGrado TR, et al. Myocardial free fatty acid and glucose use after carvedilol treatment in patients with congestive heart failure. Circulation 2001; 103: 2441-2446.
76. Mizuno Y, Yoshimura M, Yasue H, et al. Aldosterone production is activated in failing ventricle in humans. Circulation 2001; 103: 72-77.
77. Yoshimura M, Nakamura S, Ito T, et al. Expression of aldosterone synthase gene in failing human heart: quantitative analysis using modified real-time polymerase chain reaction. J Clin Endocrinol Metab 2002; 87: 3936-3940.
78. Nakamura S, Yoshimura M, Nakayama M, et al. Possible association of heart failure status with synthetic balance between aldosterone and dehydroepiandrosterone in human heart. Circulation 2004; 110: 1787-1793.
79. Cooper SA, Whaley-Connell A, Habibi J, et al. Renin-angiotensinaldosterone system and oxidative stress in cardiovascular insulin resistance. Am J Physiol Heart Circ Physiol 2007; 293: H2009-H2003.
80. Hitomi H, Kiyomoto H, Nishiyama A, et al. Aldosterone suppresses insulin signaling via the downregulation of insulin receptor substrate-1 in vascular smooth muscle cells. Hypertension 2007; 50: 750-755.
81. Wada T, Ohshima S, Fujisawa E, Koya D, Tsuneki H, Sasaoka T. Aldosterone inhibits insulin-induced glucose uptake by degradation of insulin receptor substrate (IRS) 1 and IRS2 via a reactive oxygen species-mediated pathway in 3T3-L1 adipocytes. Endocrinology 2009; 150: 1662-1669.
82. Freel EM, Tsorlalis IK, Lewsey JD, et al. Aldosterone status associated with insulin resistance in patients with heart failure--data from the ALOFT study. Heart 2009; 95: 1920-1924.
83. Pfeffer MA, Swedberg K, Granger CB, et al. Effects of candesartan on mortality and morbidity in patients with chronic heart failure: the CHARM-Overall programme. Lancet 2003; 362: 759-766.
84. Yusuf S, Sleight P, Pogue J, Bosch J, Davies R, Dagenais G. Effects of an angiotensin-converting-enzyme inhibitor, ramipril, on cardiovascular events in high-risk patients. The Heart Outcomes Prevention Evaluation Study Investigators. N Engl J Med 2000; 342: 145-153.