Differential effects of heptanoate and hexanoate on myocardial citric acid cycle intermediates following ischemia-reperfusion

Journal of Applied Physiology

Volumn 100, Issue 1, 2006, Pages 76-82

  Okere, Isidore C ^a   McElfresh, Tracy A ^a   Brunengraber, Daniel Z ^a   Martini, Wenjun ^a,b   Sterk, Joseph P ^a   Huang, Hazel ^a   Chandler, Margaret P ^a   Brunengraber, Henri ^b   Stanley, William C ^a,b,c  

^a Department of Physiology and Biophysics ^*  (United States)

^b CASE WESTERN RESERVE UNIVERSITY   (United States)

^c CASE WESTERN RESERVE UNIVERSITY SCHOOL OF MEDICINE   (United States)

Author keywords

Anaplerosis; Fatty acids; Heart; Metabolism; Mitochondria; Pyruvate dehydrogenase

Indexed keywords

CITRIC ACID; FATTY ACID; FUMARIC ACID; HEPTANOIC ACID DERIVATIVE; HEXANOIC ACID; LACTIC ACID; MALIC ACID; SUCCINIC ACID; HEXANOIC ACID DERIVATIVE;

ANIMAL EXPERIMENT; ANIMAL MODEL; ARTICLE; CITRIC ACID CYCLE; CONTROLLED STUDY; CORONARY ARTERY; DRUG EFFECT; DRUG MECHANISM; GLUCOSE OXIDATION; HEART HEMODYNAMICS; HEART MUSCLE CONTRACTILITY; ISCHEMIA; NONHUMAN; OXYGEN CONSUMPTION; PRIORITY JOURNAL; REPERFUSION; ANIMAL; COMPARATIVE STUDY; HEART; HEART CONTRACTION; HEART LEFT VENTRICLE FUNCTION; HEART MUSCLE; METABOLISM; REPERFUSION INJURY; SWINE; TREATMENT OUTCOME;

ANIMALS; CITRIC ACID CYCLE; HEART; HEPTANOATES; HEXANOIC ACIDS; MYOCARDIAL CONTRACTION; MYOCARDIUM; REPERFUSION INJURY; SWINE; TREATMENT OUTCOME; VENTRICULAR DYSFUNCTION, LEFT;

EID: 33644830537     PISSN: 87507587     EISSN: 15221601     Source Type: Journal    
DOI: 10.1152/japplphysiol.00255.2005     Document Type: Article

References (44)

1. Brunengraber H, Kelleher JK, and des Rosiers C. Applications of mass isotopomer analysis to nutrition research. Annu Rev Nutr 17: 559-596, 1997.
2. Cederblad G, Carlin JI, Constantin-Teodosiu D, Harper P, and Hultman E. Radioisotopic assays of CoASH and carnitine and their acetylated forms in human skeletal muscle. Anal Biochem 185: 274-278, 1990.
3. Chandler MP, Huang H, McElfresh TA, and Stanley WC. Increased nonoxidative glycolysis despite continued fatty acid uptake during demand-induced myocardial ischemia. Am J Physiol Heart Circ Physiol 282: H1871-H1878, 2002.
4. Churchill EN, Murriel CL, Chen CH, Mochly-Rosen D, and Szweda LI. Reperfusion-induced translocation of delta PKC to cardiac mitochondria prevents pyruvate dehydrogenase reactivation. Circ Res 97: 78-85, 2005.
5. Comte B, Vincent G, Bouchard B, Benderdour M, and des Rosiers C. Reverse flux through cardiac NADP(+)-isocitrate dehydrogenase under normoxia and ischemia. Am J Physiol Heart Circ Physiol 283: H1505-H1514, 2002.
6. 13C labeling of citrate released by perfused rat hearts. J Biol Chem 272: 26117-26124, 1997.
7. Des Rosiers C, Fernandez CA, David F, and Brunengraber H. Reversibility of the mitochondrial isocitrate dehydrogenase reaction in the perfused rat liver. Evidence from isotopomer analysis of citric acid cycle intermediates. J Biol Chem 269: 27179-27182, 1994.
8. des Rosiers C, Lloyd S, Comte B, and Chatham JC. A critical perspective of the use of (13)C-isotopomer analysis by GCMS and NMR as applied to cardiac metabolism. Metab Eng 6: 44-58, 2004.
9. Di Lisa F, Menabo R, Barbato R, and Siliprandi N. Contrasting effects of propionate and propionyl-L-carnitine on energy-linked processes in ischemic hearts. Am J Physiol Heart Circ Physiol 267: H455-H461, 1994.
10. 13C mass isotopomer distributions for natural stable isotope abundance. J Mass Spectrom 31: 255-262, 1996.
11. Gibala MJ, Young ME, and Taegtmeyer H. Anaplerosis of the citric acid cycle: role in energy metabolism of heart and skeletal muscle. Acta Physiol Scand 168: 657-665, 2000.
12. Janero DR and Hreniuk D. Suppression of TCA cycle activity in the cardiac muscle cell by hydroperoxide-induced oxidant stress. Am J Physiol Cell Physiol 270: C1735-C1742, 1996.
13. Kasumov T, Martini WZ, Reszko AE, Bian F, Pierce BA, David F, Roe CR, and Brunengraber H. Assay of the concentration and (13)C isotopic enrichment of propionyl-CoA, methylmalonyl-CoA, and succinyl-CoA by gas chromatography-mass spectrometry. Anal Biochem 305: 90-96, 2002.
14. Kornberg HL. Anaplerotic sequences and their role in metabolism. In: Essays in Biochemistry, edited by Campbell PN and Marshall RD. London: Academic, 1966, p. 1-31.
15. Laplante A, Comte B, and des Rosiers C. Assay of blood and tissue oxaloacetate and alpha-ketoglutarate by isotope dilution gas chromatography-mass spectrometry. Anal Biochem 224: 580-587, 1995.
16. 13C mass isotopomer study. Am J Physiol Endocrinol Metab 272: E74-E82, 1997.
17. Liedtke AJ, Hacker T, Renstrom B, and Nellis SH. Anaplerotic effects of propionate on oxidations of acetate and long-chain fatty acids. Am J Physiol Heart Circ Physiol 270: H2197-H2203, 1996.
18. Lopaschuk GD, Wambolt RB, and Barr RL. An imbalance between glycolysis and glucose oxidation is a possible explanation for the detrimental effects of high levels of fatty acids during aerobic reperfusion of ischemic hearts. J Pharmacol Exp Ther 264: 135-144, 1993.
19. Lucas DT and Szweda LI. Declines in mitochondrial respiration during cardiac reperfusion: age-dependent inactivation of alpha-ketoglutarate dehydrogenase. Proc Natl Acad Sci USA 96: 6689-6693, 1999.
20. Mallet RT. Pyruvate: metabolic protector of cardiac performance. Proc Soc Exp Biol Med 223: 136-148, 2000.
21. 13C NMR spectroscopy. J Biol Chem 263: 6964-6971, 1988.
22. Martini WZ, Stanley WC, Huang H, des Rosiers C, Hoppel CL, and Brunengraber H. Quantitative assessment of anaplerosis from propionate in pig heart in vivo. Am J Physiol Endocrinol Metab 284: E351-E356, 2003.
23. Myears DW, Sobel BE, and Bergmann SR. Substrate use in ischemic and reperfused canine myocardium: quantitative considerations. Am J Physiol Heart Circ Physiol 253: H107-H114, 1987.
24. Nulton-Persson AC and Szweda LI. Modulation of mitochondrial function by hydrogen peroxide. J Biol Chem 276: 23357-23361, 2001.
25. Panchal AR, Comte B, Huang H, Dudar B, Roth B, Chandler M, des Rosiers C, Brunengraber H, and Stanley WC. Acute hibernation decreases myocardial pyruvate carboxylation and citrate release. Am J Physiol Heart Circ Physiol 281: H1613-H1620, 2001.
26. Panchal AR, Comte B, Huang H, Kerwin T, Darvish A, des Rosiers C, Brunengraber H, and Stanley WC. Partitioning of pyruvate between oxidation and anaplerosis in swine hearts. Am J Physiol Heart Circ Physiol 279: H2390-H2398, 2000.
27. Renstrom B, Nellis SH, and Liedtke AJ. Metabolic oxidation of glucose during early myocardial reperfusion. Circ Res 65: 1094-1101, 1989.
28. Reszko AE, Kasumov T, Pierce BA, David F, Hoppel CL, Stanley WC, des Rosiers C, and Brunengraber H. Assessing the reversibility of the anaplerotic reactions of the propionyl-CoA pathway in heart and liver. J Biol Chem 278: 34959-34965, 2003.
29. Roe CR, Sweetman L, Roe DS, David F, and Brunengraber H. Treatment of cardiomyopathy and rhabdomyolysis in long-chain fat oxidation disorders using an anaplerotic odd-chain triglyceride. J Clin Invest 110: 259-269, 2002.
30. Russell RR III and Taegtmeyer H. Changes in citric acid cycle flux and anaplerosis antedate the functional decline in isolated rat hearts utilizing acetoacetate. J Clin Invest 87: 384-390, 1991.
31. Russell RR III and Taegtmeyer H. Pyruvate carboxylation prevents the decline in contractile function of rat hearts oxidizing acetoacetate. Am J Physiol Heart Circ Physiol 261: H1756-H1762, 1991.
32. Sadek HA, Humphries KM, Szweda PA, and Szweda LI. Selective inactivation of redox-sensitive mitochondrial enzymes during cardiac reperfusion. Arch Biochem Biophys 406: 222-228, 2002.
33. Schoder H, Knight RJ, Kofoed KF, Schelbert HR, and Buxton DB. Regulation of pyruvate dehydrogenase activity and glucose metabolism in post-ischaemic myocardium. Biochim Biophys Acta 1406: 62-72, 1998.
34. Sharma N, Okere IC, Brunengraber DZ, McElfresh TA, King KL, Sterk JP, Huang H, Chandler MP, and Stanley WC. Regulation of pyruvate dehydrogenase activity and citric acid cycle intermediates during high cardiac power generation. J Physiol 562: 593-603, 2005.
35. Stanley WC, Hernandez LA, Spires D, Bringas J, Wallace S, and McCormack JG. Pyruvate dehydrogenase activity and malonyl CoA levels in normal and ischemic swine myocardium: effects of dichloroacetate. J Mol Cell Cardiol 28: 905-914, 1996.
36. Stanley WC, Kivilo KM, Panchal AR, Hallowell PH, Bomont C, Kasumov T, and Brunengraber H. Post-ischemic treatment with dipyruvyl-acetyl-glycerol decreases myocardial infarct size in the pig. Cardiovasc Drugs Ther 17: 209-216, 2003.
37. Stanley WC, Lopaschuk GD, Hall JL, and McCormack JG. Regulation of myocardial carbohydrate metabolism under normal and ischaemic conditions. Potential for pharmacological interventions. Cardiovasc Res 33: 243-257, 1997.
38. Sterk JP, Stanley WC, Hoppel CL, and Kerner J. A radiochemical pyruvate dehydrogenase assay: activity in heart. Anal Biochem 313: 179-182, 2003.
39. Sundqvist KE, Vuorinen KH, Peuhkurinen KJ, and Hassinen IE. Metabolic effects of propionate, hexanoate and propionylcarnitine in normoxia, ischaemia and reperfusion. Does an anaplerotic substrate protect the ischaemic myocardium? Eur Heart J 15: 561-570, 1994.
40. Thomassen A, Nielsen TT, Bagger JP, Pedersen AK, and Henningsen P. Antiischemic and metabolic effects of glutamate during pacing in patients with stable angina pectoris secondary to either coronary artery disease or syndrome X. Am J Cardiol 68: 291-295, 1991.
41. Thomassen AR. Myocardial uptake and effects of glutamate during non-ischaemic and ischaemic conditions. A clinical study with special reference to possible interrelationships between glutamate and myocardial utilization of carbohydrate substrates. Dan Med Bull 39: 471-488, 1992.
42. Thomassen AR, Nielsen TT, Bagger JP, and Henningsen P. Myocardial exchanges of glutamate, alanine and citrate in controls and patients with coronary artery disease. Clin Sci (Lond) 64: 33-40, 1983.
43. Wisneski JA, Gertz EW, Neese RA, Gruenke LD, Morris DL, and Craig JC. Metabolic fate of extracted glucose in normal human myocardium. J Clin Invest 76: 1819-1827, 1985.
44. 14C-labeled substrates in humans. J Clin Invest 79: 359-366, 1987.