Mild Type 2 Diabetes Mellitus Reduces the Susceptibility of the Heart to Ischemia/Reperfusion Injury: Identification of Underlying Gene Expression Changes

Journal of Diabetes Research

Volumn 2015, Issue , 2015, Pages

  Korkmaz Icöz, Sevil ^a   Lehner, Alice ^a   Li, Shiliang ^a   Vater, Adrian ^a   Radovits, Tamás ^b   Hegedus, Péter ^a,b   Ruppert, Mihály ^a   Brlecic, Paige ^a   Zorn, Markus ^a   Karck, Matthias ^a   Szabó, Gábor ^a  

^a UNIVERSITY OF HEIDELBERG   (Germany)

^b SEMMELWEIS UNIVERSITY   (Hungary)

Author keywords

[No Author keywords available]

Indexed keywords

GLUCOSE; PHOSPHATIDYLINOSITOL 3 KINASE; GLUCOSE BLOOD LEVEL; MUSCLE PROTEIN;

ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; ARTICLE; CONTROLLED STUDY; DISEASE PREDISPOSITION; DOWN REGULATION; FIBROSING ALVEOLITIS; GENE EXPRESSION; GLUCOSE BLOOD LEVEL; HEART MUSCLE ISCHEMIA; HEART PROTECTION; HEART VENTRICLE HYPERTROPHY; IN VIVO STUDY; LEFT ANTERIOR DESCENDING CORONARY ARTERY; MALE; NON INSULIN DEPENDENT DIABETES MELLITUS; NONHUMAN; PRIORITY JOURNAL; RAT; REPERFUSION INJURY; UPREGULATION; ANALYSIS; ANIMAL; BLOOD; CARDIAC MUSCLE; CARDIOMEGALY; COMPLICATION; DIABETIC CARDIOMYOPATHY; FIBROSIS; GENE EXPRESSION PROFILING; GENE EXPRESSION REGULATION; GENETICS; HEART; HEART INFARCTION; INBRED RAT STRAIN; METABOLISM; MYOCARDIAL ISCHEMIA REPERFUSION INJURY; PATHOLOGY; PATHOPHYSIOLOGY; RANDOMIZATION; SEVERITY OF ILLNESS INDEX; WISTAR RAT;

ANIMALS; BLOOD GLUCOSE; CARDIOMEGALY; DIABETES MELLITUS, TYPE 2; DIABETIC CARDIOMYOPATHIES; DISEASE SUSCEPTIBILITY; FIBROSIS; GENE EXPRESSION PROFILING; GENE EXPRESSION REGULATION; HEART; MALE; MUSCLE PROTEINS; MYOCARDIAL INFARCTION; MYOCARDIAL ISCHEMIA; MYOCARDIAL REPERFUSION INJURY; MYOCARDIUM; RANDOM ALLOCATION; RATS, INBRED STRAINS; RATS, WISTAR; SEVERITY OF ILLNESS INDEX;

EID: 84937010876     PISSN: 23146745     EISSN: 23146753     Source Type: Journal    
DOI: 10.1155/2015/396414     Document Type: Article

References (33)

1. G. C. Fonarow and P. Srikanthan, "Diabetic cardiomyopathy," Endocrinology and Metabolism Clinics of North America, vol. 35, no. 3, pp. 575-599, 2006.
2. D. L. Severson, "Diabetic cardiomyopathy: recent evidence from mouse models of type 1 and type 2 diabetes," Canadian Journal of Physiology and Pharmacology, vol. 82, no. 10, pp. 813-823, 2004.
3. M. J. Garcia, P.M. McNamara, T. Gordon, and W. B. Kannell, "Morbidity and mortality in diabetics in the Framingham population. Sixteen year follow-up study," Diabetes, vol. 23, no. 2, pp. 105-111, 1974.
4. K. J. Mukamal, R. W. Nesto, M. C. Cohen et al., "Impact of diabetes on long-term survival after acute myocardial infarction: comparability of riskwith priormyocardial infarction," Diabetes Care, vol. 24, no. 8, pp. 1422-1427, 2001.
5. P. H. Stone, J. E. Muller, T. Hartwell et al., "The effect of diabetes mellitus on prognosis and serial left ventricular function after acute myocardial infarction: contribution of both coronary disease and diastolic left ventricular dysfunction to the adverse prognosis. The MILIS Study Group," Journal of the American College of Cardiology, vol. 14, no. 1, pp. 49-57, 1989.
6. J. R. Alegria, T. D. Miller, R. J. Gibbons, Q.-L. Yi, and S. Yusuf, "Infarct size, ejection fraction, and mortality in diabetic patients with acute myocardial infarction treated with thrombolytic therapy," American Heart Journal, vol. 154, no. 4, pp. 743-750, 2007.
7. S. P. Marso, T. Miller, B. D. Rutherford et al., "Comparison of myocardial reperfusion in patients undergoing percutaneous coronary intervention in ST-segment elevation acute myocardial infarction with versus without diabetes mellitus (from the EMERALD Trial)," American Journal of Cardiology, vol. 100, no. 2, pp. 206-210, 2007.
8. D. Feuvray and G.D. Lopaschuk, "Controversies on the sensitivity of the diabetic heart to ischemic injury: the sensitivity of the diabetic heart to ischemic injury is decreased," Cardiovascular Research, vol. 34, no. 1, pp. 113-120, 1997.
9. D. J. Paulson, "The diabetic heart is more sensitive to ischemic injury," Cardiovascular Research, vol. 34, no. 1, pp. 104-112, 1997.
10. C. Malfitano, A. L. de Souza Junior, and M. C. Irigoyen, "Impact of conditioning hyperglycemic on myocardial infarction rats: cardiac cell survival factors," World Journal of Cardiology, vol. 6, no. 6, pp. 449-454, 2014.
11. Y. Goto, M. Kakizaki, and N. Masaki, "Production of spontaneous diabetic rats by repetition of selective breeding," Tohoku Journal of Experimental Medicine, vol. 119, no. 1, pp. 85-90, 1976.
12. G. Hadour, R. Ferrera, L. Sebbag, R. Forrat, J. Delaye, and M. de Lorgeril, "Improved myocardial tolerance to ischaemia in the diabetic rabbit," Journal of Molecular and Cellular Cardiology, vol. 30, no. 9, pp. 1869-1875, 1998.
13. S. B. Kristiansen, B. Løfgren, N. B. Støttrup et al., "Ischaemic preconditioning does not protect the heart in obese and lean animal models of Type 2 diabetes," Diabetologia, vol. 47, no. 10, pp. 1716-1721, 2004.
14. M. Desrois, K. Clarke, C. Lan et al., "Upregulation of eNOS and unchanged energymetabolism in increased susceptibility of the aging type 2 diabetic GK rat heart to ischemic injury," American Journal of Physiology-Heart and Circulatory Physiology, vol. 299, no. 5, pp. H1679-H1686, 2010.
15. C. di Filippo, R. Marfella, S. Cuzzocrea et al., "Hyperglycemia in streptozotocin-induced diabetic rat increases infarct size associated with low levels of myocardial HO-1 during ischemia/reperfusion," Diabetes, vol. 54, no. 3, pp. 803-810, 2005.
16. R. Marfella, M.D'Amico, C. Di Filippo et al., "Myocardial infarction in diabetic rats: role of hyperglycaemia on infarct size and early expression of hypoxia-inducible factor 1," Diabetologia, vol. 45, no. 8, pp. 1172-1181, 2002.
17. A. A. Bulhak, C. Jung, C.-G. Östenson, J. O. Lundberg, P.-O. Sjoquist, and J. Pernow, "PPAR-α activation protects the type 2 diabetic myocardium against ischemia-reperfusion injury: Involvement of the PI3-kinase/Akt and NOpathway," American Journal of Physiology-Heart and Circulatory Physiology, vol. 296, no. 3, pp. H719-H727, 2009.
18. S. Matsumoto, S. Cho, S. Tosaka et al., "Pharmacological preconditioning in type 2 diabetic rat hearts: the roles of mitochondrial ATP-sensitive potassiumchannels and the phosphatidylinositol 3-kinase-Akt pathway," Cardiovascular Drugs and Therapy, vol. 23, no. 4, pp. 263-270, 2009.
19. H. J. Whittington, G. G. Babu, M. M. Mocanu, D. M. Yellon, and D. J. Hausenloy, "The diabetic heart: too sweet for its own good?" Cardiology Research and Practice, vol. 2012, Article ID 845698, 15 pages, 2012.
20. M. M. Galagudza, M. K. Nekrasova, A. V. Syrenskii, and E. M. Nifontov, "Resistance of the myocardium to ischemia and the efficacy of ischemic preconditioning in experimental diabetes mellitus," Neuroscience and Behavioral Physiology, vol. 37, no. 5, pp. 489-493, 2007.
21. + exchange during ischaemia and reperfusion of normal and diabetic rat hearts," Cardiovascular Research, vol. 24, no. 11, pp. 873-878, 1990.
22. S. B. Kristiansen, B. Lofgren, J. M. Nielsen et al., "Comparison of two sulfonylureas with high and low myocardial K(ATP) channel affinity on myocardial infarct size and metabolism in a rat model of type 2 diabetes," Diabetologia, vol. 54, no. 2, pp. 451-458, 2011.
23. C. Lajoie, A. Calderone, F. Trudeau et al., "Exercise training attenuated the PKB and GSK-3 dephosphorylation in the myocardium of ZDF rats," Journal of Applied Physiology, vol. 96, no. 5, pp. 1606-1612, 2004.
24. M. V. Cohen, "Free radicals in ischemic and reperfusion myocardial injury: is this the time for clinical trials?" Annals of Internal Medicine, vol. 111, no. 11, pp. 918-931, 1989.
25. S. W. Werns and B. R. Lucchesi, "Free radicals and ischemic tissue injury," Trends in Pharmacological Sciences, vol. 11, no. 4, pp. 161-166, 1990.
26. G. Zeng, F. H. Nystrom, L. V. Ravichandran et al., "Roles for insulin receptor, PI3-kinase, and Akt in insulin-signaling pathways related to production of nitric oxide in human vascular endothelial cells," Circulation, vol. 101, no. 13, pp. 1539-1545, 2000.
27. T.F. Franke, D. R. Kaplan, and L. C. Cantley, "PI3K: downstream AKTion blocks apoptosis," Cell, vol. 88, no. 4, pp. 435-437, 1997.
28. Y. Qi, Z. Xu, Q. Zhu et al., "Myocardial loss of IRS1 and IRS2 causes heart failure and is controlled by p38α MAPK during insulin resistance," Diabetes, vol. 62, no. 11, pp. 3887-3900, 2013.
29. Z. Lu, Y.-P. Jiang, W. Wang et al., "Loss of cardiac phosphoinositide 3-kinase p110α results in contractile dysfunction," Circulation, vol. 120, no. 4, pp. 318-325, 2009.
30. Y. Fujio, T. Nguyen, D. Wencker, R. N. Kitsis, and K. Walsh, "Akt promotes survival of cardiomyocytes in vitro and protects against lschemia-reperfusion injury in mouse heart," Circulation, vol. 101, no. 6, pp. 660-667, 2000.
31. J. Jager, T. Grémeaux, M. Cormont, Y. le Marchand-Brustel, and J.-F. Tanti, "Interleukin-1beta-induced insulin resistance in adipocytes through down-regulation of insulin receptor substrate-1 expression," Endocrinology, vol. 148, no. 1, pp. 241-251, 2007.
32. B. Swynghedauw, "Molecular mechanisms of myocardial remodeling," Physiological Reviews, vol. 79, no. 1, pp. 215-262, 1999.
33. D. J. Hearse and R. Bolli, "Reperfusion induced injury: manifestations, mechanisms, and clinical relevance," Cardiovascular Research, vol. 26, no. 2, pp. 101-108, 1992.