Skip to main content
Erschienen in: Reviews in Endocrine and Metabolic Disorders 1/2010

01.03.2010

Diabetic cardiomyopathy, causes and effects

verfasst von: Sihem Boudina, Evan Dale Abel

Erschienen in: Reviews in Endocrine and Metabolic Disorders | Ausgabe 1/2010

Einloggen, um Zugang zu erhalten

Abstract

Diabetes is associated with increased incidence of heart failure even after controlling for coronary artery disease and hypertension. Thus, as diabetic cardiomyopathy has become an increasingly recognized entity among clinicians, a better understanding of its pathophysiology is necessary for early diagnosis and the development of treatment strategies for diabetes-associated cardiovascular dysfunction. We will review recent basic and clinical research into the manifestations and the pathophysiological mechanisms of diabetic cardiomyopathy. The discussion will be focused on the structural, functional and metabolic changes that occur in the myocardium in diabetes and how these changes may contribute to the development of diabetic cardiomyopathy in affected humans and relevant animal models.
Literatur
1.
Zurück zum Zitat Rubler S, Dlugash J, Yuceoglu YZ, Kumral T, Branwood AW, Grishman A. New type of cardiomyopathy associated with diabetic glomerulosclerosis. Am J Cardiol. 1972;30(6):595–602.CrossRefPubMed Rubler S, Dlugash J, Yuceoglu YZ, Kumral T, Branwood AW, Grishman A. New type of cardiomyopathy associated with diabetic glomerulosclerosis. Am J Cardiol. 1972;30(6):595–602.CrossRefPubMed
2.
Zurück zum Zitat Hayat SA, Patel B, Khattar RS, Malik RA. Diabetic cardiomyopathy: mechanisms, diagnosis and treatment. Clin Sci (Lond) 2004;107(6):539–57.CrossRef Hayat SA, Patel B, Khattar RS, Malik RA. Diabetic cardiomyopathy: mechanisms, diagnosis and treatment. Clin Sci (Lond) 2004;107(6):539–57.CrossRef
3.
Zurück zum Zitat Aneja A, Tang WH, Bansilal S, Garcia MJ, Farkouh ME. Diabetic cardiomyopathy: insights into pathogenesis, diagnostic challenges, and therapeutic options. Am J Med. 2008;121(9):748–57.CrossRefPubMed Aneja A, Tang WH, Bansilal S, Garcia MJ, Farkouh ME. Diabetic cardiomyopathy: insights into pathogenesis, diagnostic challenges, and therapeutic options. Am J Med. 2008;121(9):748–57.CrossRefPubMed
4.
Zurück zum Zitat Galderisi M, Anderson KM, Wilson PW, Levy D. Echocardiographic evidence for the existence of a distinct diabetic cardiomyopathy (the Framingham Heart Study). Am J Cardiol. 1991;68(1):85–9.CrossRefPubMed Galderisi M, Anderson KM, Wilson PW, Levy D. Echocardiographic evidence for the existence of a distinct diabetic cardiomyopathy (the Framingham Heart Study). Am J Cardiol. 1991;68(1):85–9.CrossRefPubMed
5.
Zurück zum Zitat Devereux RB, Roman MJ, Paranicas M, O’Grady MJ, Lee ET, Welty TK, et al. Impact of diabetes on cardiac structure and function: the strong heart study. Circulation 2000;101(19):2271–6.PubMed Devereux RB, Roman MJ, Paranicas M, O’Grady MJ, Lee ET, Welty TK, et al. Impact of diabetes on cardiac structure and function: the strong heart study. Circulation 2000;101(19):2271–6.PubMed
6.
Zurück zum Zitat Eguchi K, Boden-Albala B, Jin Z, Rundek T, Sacco RL, Homma S, et al. Association between diabetes mellitus and left ventricular hypertrophy in a multiethnic population. Am J Cardiol. 2008;101(12):1787–91.CrossRefPubMed Eguchi K, Boden-Albala B, Jin Z, Rundek T, Sacco RL, Homma S, et al. Association between diabetes mellitus and left ventricular hypertrophy in a multiethnic population. Am J Cardiol. 2008;101(12):1787–91.CrossRefPubMed
7.
Zurück zum Zitat Rerkpattanapipat P, D’Agostino Jr RB, Link KM, Shahar E, Lima JA, Bluemke DA, et al. Location of arterial stiffening differs in those with impaired fasting glucose versus diabetes: implications for left ventricular hypertrophy from the Multi-Ethnic Study of Atherosclerosis. Diabetes 2009;58(4):946–53.CrossRefPubMed Rerkpattanapipat P, D’Agostino Jr RB, Link KM, Shahar E, Lima JA, Bluemke DA, et al. Location of arterial stiffening differs in those with impaired fasting glucose versus diabetes: implications for left ventricular hypertrophy from the Multi-Ethnic Study of Atherosclerosis. Diabetes 2009;58(4):946–53.CrossRefPubMed
8.
Zurück zum Zitat Woodiwiss AJ, Libhaber CD, Majane OH, Libhaber E, Maseko M, Norton GR. Obesity promotes left ventricular concentric rather than eccentric geometric remodeling and hypertrophy independent of blood pressure. Am J Hypertens. 2008;21(10):1144–51.CrossRefPubMed Woodiwiss AJ, Libhaber CD, Majane OH, Libhaber E, Maseko M, Norton GR. Obesity promotes left ventricular concentric rather than eccentric geometric remodeling and hypertrophy independent of blood pressure. Am J Hypertens. 2008;21(10):1144–51.CrossRefPubMed
9.
Zurück zum Zitat Barouch LA, Berkowitz DE, Harrison RW, O’Donnell CP, Hare JM. Disruption of leptin signaling contributes to cardiac hypertrophy independently of body weight in mice. Circulation 2003;108(6):754–9.CrossRefPubMed Barouch LA, Berkowitz DE, Harrison RW, O’Donnell CP, Hare JM. Disruption of leptin signaling contributes to cardiac hypertrophy independently of body weight in mice. Circulation 2003;108(6):754–9.CrossRefPubMed
10.
Zurück zum Zitat Xu FP, Chen MS, Wang YZ, Yi Q, Lin SB, Chen AF, et al. Leptin induces hypertrophy via endothelin-1-reactive oxygen species pathway in cultured neonatal rat cardiomyocytes. Circulation 2004;110(10):1269–75.CrossRefPubMed Xu FP, Chen MS, Wang YZ, Yi Q, Lin SB, Chen AF, et al. Leptin induces hypertrophy via endothelin-1-reactive oxygen species pathway in cultured neonatal rat cardiomyocytes. Circulation 2004;110(10):1269–75.CrossRefPubMed
11.
Zurück zum Zitat Kim M, Oh JK, Sakata S, Liang I, Park W, Hajjar RJ, et al. Role of resistin in cardiac contractility and hypertrophy. J Mol Cell Cardiol. 2008;45(2):270–80.CrossRefPubMed Kim M, Oh JK, Sakata S, Liang I, Park W, Hajjar RJ, et al. Role of resistin in cardiac contractility and hypertrophy. J Mol Cell Cardiol. 2008;45(2):270–80.CrossRefPubMed
12.
Zurück zum Zitat Bahrami H, Bluemke DA, Kronmal R, Bertoni AG, Lloyd-Jones DM, Shahar E, et al. Novel metabolic risk factors for incident heart failure and their relationship with obesity: the MESA (Multi-Ethnic Study of Atherosclerosis) study. J Am Coll Cardiol. 2008;51(18):1775–83.CrossRefPubMed Bahrami H, Bluemke DA, Kronmal R, Bertoni AG, Lloyd-Jones DM, Shahar E, et al. Novel metabolic risk factors for incident heart failure and their relationship with obesity: the MESA (Multi-Ethnic Study of Atherosclerosis) study. J Am Coll Cardiol. 2008;51(18):1775–83.CrossRefPubMed
13.
Zurück zum Zitat Karason K, Sjostrom L, Wallentin I, Peltonen M. Impact of blood pressure and insulin on the relationship between body fat and left ventricular structure. Eur Heart J. 2003;24(16):1500–5.CrossRefPubMed Karason K, Sjostrom L, Wallentin I, Peltonen M. Impact of blood pressure and insulin on the relationship between body fat and left ventricular structure. Eur Heart J. 2003;24(16):1500–5.CrossRefPubMed
14.
Zurück zum Zitat Ingelsson E, Sundstrom J, Arnlov J, Zethelius B, Lind L. Insulin resistance and risk of congestive heart failure. Jama 2005;294(3):334–41.CrossRefPubMed Ingelsson E, Sundstrom J, Arnlov J, Zethelius B, Lind L. Insulin resistance and risk of congestive heart failure. Jama 2005;294(3):334–41.CrossRefPubMed
15.
Zurück zum Zitat Cook SA, Varela-Carver A, Mongillo M, Kleinert C, Khan MT, Leccisotti L, Strickland N, Matsui T, Das S, Rosenzweig A et al: Abnormal myocardial insulin signalling in type 2 diabetes and left-ventricular dysfunction. Eur Heart J. 2009. Cook SA, Varela-Carver A, Mongillo M, Kleinert C, Khan MT, Leccisotti L, Strickland N, Matsui T, Das S, Rosenzweig A et al: Abnormal myocardial insulin signalling in type 2 diabetes and left-ventricular dysfunction. Eur Heart J. 2009.
16.
Zurück zum Zitat Belke DD, Betuing S, Tuttle MJ, Graveleau C, Young ME, Pham M, et al. Insulin signaling coordinately regulates cardiac size, metabolism, and contractile protein isoform expression. J Clin Invest. 2002;109(5):629–39.PubMed Belke DD, Betuing S, Tuttle MJ, Graveleau C, Young ME, Pham M, et al. Insulin signaling coordinately regulates cardiac size, metabolism, and contractile protein isoform expression. J Clin Invest. 2002;109(5):629–39.PubMed
17.
Zurück zum Zitat Wende AR, Abel ED: Lipotoxicity in the heart. Biochim Biophys Acta 2009. Wende AR, Abel ED: Lipotoxicity in the heart. Biochim Biophys Acta 2009.
18.
Zurück zum Zitat Regan TJ, Lyons MM, Ahmed SS, Levinson GE, Oldewurtel HA, Ahmad MR, et al. Evidence for cardiomyopathy in familial diabetes mellitus. J Clin Invest. 1977;60(4):884–99.CrossRefPubMed Regan TJ, Lyons MM, Ahmed SS, Levinson GE, Oldewurtel HA, Ahmad MR, et al. Evidence for cardiomyopathy in familial diabetes mellitus. J Clin Invest. 1977;60(4):884–99.CrossRefPubMed
19.
Zurück zum Zitat Sharma S, Adrogue JV, Golfman L, Uray I, Lemm J, Youker K, et al. Intramyocardial lipid accumulation in the failing human heart resembles the lipotoxic rat heart. Faseb J. 2004;18(14):1692–700.CrossRefPubMed Sharma S, Adrogue JV, Golfman L, Uray I, Lemm J, Youker K, et al. Intramyocardial lipid accumulation in the failing human heart resembles the lipotoxic rat heart. Faseb J. 2004;18(14):1692–700.CrossRefPubMed
20.
Zurück zum Zitat McGavock JM, Lingvay I, Zib I, Tillery T, Salas N, Unger R, et al. Cardiac steatosis in diabetes mellitus: a 1H-magnetic resonance spectroscopy study. Circulation 2007;116(10):1170–5.CrossRefPubMed McGavock JM, Lingvay I, Zib I, Tillery T, Salas N, Unger R, et al. Cardiac steatosis in diabetes mellitus: a 1H-magnetic resonance spectroscopy study. Circulation 2007;116(10):1170–5.CrossRefPubMed
21.
Zurück zum Zitat Rijzewijk LJ, van der Meer RW, Smit JW, Diamant M, Bax JJ, Hammer S, et al. Myocardial steatosis is an independent predictor of diastolic dysfunction in type 2 diabetes mellitus. J Am Coll Cardiol. 2008;52(22):1793–9.CrossRefPubMed Rijzewijk LJ, van der Meer RW, Smit JW, Diamant M, Bax JJ, Hammer S, et al. Myocardial steatosis is an independent predictor of diastolic dysfunction in type 2 diabetes mellitus. J Am Coll Cardiol. 2008;52(22):1793–9.CrossRefPubMed
22.
Zurück zum Zitat van der Meer RW, Rijzewijk LJ, de Jong HW, Lamb HJ, Lubberink M, Romijn JA, et al. Pioglitazone improves cardiac function and alters myocardial substrate metabolism without affecting cardiac triglyceride accumulation and high-energy phosphate metabolism in patients with well-controlled type 2 diabetes mellitus. Circulation 2009;119(15):2069–77.CrossRefPubMed van der Meer RW, Rijzewijk LJ, de Jong HW, Lamb HJ, Lubberink M, Romijn JA, et al. Pioglitazone improves cardiac function and alters myocardial substrate metabolism without affecting cardiac triglyceride accumulation and high-energy phosphate metabolism in patients with well-controlled type 2 diabetes mellitus. Circulation 2009;119(15):2069–77.CrossRefPubMed
23.
Zurück zum Zitat Abel ED, Litwin SE, Sweeney G. Cardiac remodeling in obesity. Physiol Rev. 2008;88(2):389–419.CrossRefPubMed Abel ED, Litwin SE, Sweeney G. Cardiac remodeling in obesity. Physiol Rev. 2008;88(2):389–419.CrossRefPubMed
24.
25.
Zurück zum Zitat Chiu HC, Kovacs A, Ford DA, Hsu FF, Garcia R, Herrero P, et al. A novel mouse model of lipotoxic cardiomyopathy. J Clin Invest. 2001;107(7):813–22.CrossRefPubMed Chiu HC, Kovacs A, Ford DA, Hsu FF, Garcia R, Herrero P, et al. A novel mouse model of lipotoxic cardiomyopathy. J Clin Invest. 2001;107(7):813–22.CrossRefPubMed
26.
Zurück zum Zitat Yagyu H, Chen G, Yokoyama M, Hirata K, Augustus A, Kako Y, et al. Lipoprotein lipase (LpL) on the surface of cardiomyocytes increases lipid uptake and produces a cardiomyopathy. J Clin Invest. 2003;111(3):419–26.PubMed Yagyu H, Chen G, Yokoyama M, Hirata K, Augustus A, Kako Y, et al. Lipoprotein lipase (LpL) on the surface of cardiomyocytes increases lipid uptake and produces a cardiomyopathy. J Clin Invest. 2003;111(3):419–26.PubMed
27.
Zurück zum Zitat Listenberger LL, Ory DS, Schaffer JE. Palmitate-induced apoptosis can occur through a ceramide-independent pathway. J Biol Chem. 2001;276(18):14890–5.CrossRefPubMed Listenberger LL, Ory DS, Schaffer JE. Palmitate-induced apoptosis can occur through a ceramide-independent pathway. J Biol Chem. 2001;276(18):14890–5.CrossRefPubMed
28.
Zurück zum Zitat Park TS, Hu Y, Noh HL, Drosatos K, Okajima K, Buchanan J, et al. Ceramide is a cardiotoxin in lipotoxic cardiomyopathy. J Lipid Res. 2008;49(10):2101–12.CrossRefPubMed Park TS, Hu Y, Noh HL, Drosatos K, Okajima K, Buchanan J, et al. Ceramide is a cardiotoxin in lipotoxic cardiomyopathy. J Lipid Res. 2008;49(10):2101–12.CrossRefPubMed
29.
Zurück zum Zitat Ostrander DB, Sparagna GC, Amoscato AA, McMillin JB, Dowhan W. Decreased cardiolipin synthesis corresponds with cytochrome c release in palmitate-induced cardiomyocyte apoptosis. J Biol Chem. 2001;276(41):38061–7.PubMed Ostrander DB, Sparagna GC, Amoscato AA, McMillin JB, Dowhan W. Decreased cardiolipin synthesis corresponds with cytochrome c release in palmitate-induced cardiomyocyte apoptosis. J Biol Chem. 2001;276(41):38061–7.PubMed
30.
Zurück zum Zitat Borradaile NM, Han X, Harp JD, Gale SE, Ory DS, Schaffer JE. Disruption of endoplasmic reticulum structure and integrity in lipotoxic cell death. J Lipid Res. 2006;47(12):2726–37.CrossRefPubMed Borradaile NM, Han X, Harp JD, Gale SE, Ory DS, Schaffer JE. Disruption of endoplasmic reticulum structure and integrity in lipotoxic cell death. J Lipid Res. 2006;47(12):2726–37.CrossRefPubMed
31.
Zurück zum Zitat Brookheart RT, Michel CI, Listenberger LL, Ory DS, Schaffer JE. The non-coding RNA gadd7 is a regulator of lipid-induced oxidative and endoplasmic reticulum stress. J Biol Chem. 2009;284(12):7446–54.CrossRefPubMed Brookheart RT, Michel CI, Listenberger LL, Ory DS, Schaffer JE. The non-coding RNA gadd7 is a regulator of lipid-induced oxidative and endoplasmic reticulum stress. J Biol Chem. 2009;284(12):7446–54.CrossRefPubMed
32.
Zurück zum Zitat Boudina S, Sena S, Theobald H, Sheng X, Wright JJ, Hu XX, 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(10):2457–66.CrossRefPubMed Boudina S, Sena S, Theobald H, Sheng X, Wright JJ, Hu XX, 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(10):2457–66.CrossRefPubMed
33.
Zurück zum Zitat Bugger H, Boudina S, Hu XX, Tuinei J, Zaha VG, Theobald HA, et al. Type 1 diabetic akita mouse hearts are insulin sensitive but manifest structurally abnormal mitochondria that remain coupled despite increased uncoupling protein 3. Diabetes 2008;57(11):2924–32.CrossRefPubMed Bugger H, Boudina S, Hu XX, Tuinei J, Zaha VG, Theobald HA, et al. Type 1 diabetic akita mouse hearts are insulin sensitive but manifest structurally abnormal mitochondria that remain coupled despite increased uncoupling protein 3. Diabetes 2008;57(11):2924–32.CrossRefPubMed
34.
Zurück zum Zitat Boudina S, Bugger H, Sena S, O’Neill BT, Zaha VG, Ilkun O, et al. Contribution of impaired myocardial insulin signaling to mitochondrial dysfunction and oxidative stress in the heart. Circulation 2009;119(9):1272–83.CrossRefPubMed Boudina S, Bugger H, Sena S, O’Neill BT, Zaha VG, Ilkun O, et al. Contribution of impaired myocardial insulin signaling to mitochondrial dysfunction and oxidative stress in the heart. Circulation 2009;119(9):1272–83.CrossRefPubMed
35.
Zurück zum Zitat Li L, Renier G. Activation of nicotinamide adenine dinucleotide phosphate (reduced form) oxidase by advanced glycation end products links oxidative stress to altered retinal vascular endothelial growth factor expression. Metabolism 2006;55(11):1516–23.CrossRefPubMed Li L, Renier G. Activation of nicotinamide adenine dinucleotide phosphate (reduced form) oxidase by advanced glycation end products links oxidative stress to altered retinal vascular endothelial growth factor expression. Metabolism 2006;55(11):1516–23.CrossRefPubMed
36.
Zurück zum Zitat Serpillon S, Floyd BC, Gupte RS, George S, Kozicky M, Neito V, et al. Superoxide production by NAD(P)H oxidase and mitochondria is increased in genetically obese and hyperglycemic rat heart and aorta before the development of cardiac dysfunction. The role of glucose-6-phosphate dehydrogenase-derived NADPH. Am J Physiol Heart Circ Physiol. 2009;297(1):H153–62.CrossRefPubMed Serpillon S, Floyd BC, Gupte RS, George S, Kozicky M, Neito V, et al. Superoxide production by NAD(P)H oxidase and mitochondria is increased in genetically obese and hyperglycemic rat heart and aorta before the development of cardiac dysfunction. The role of glucose-6-phosphate dehydrogenase-derived NADPH. Am J Physiol Heart Circ Physiol. 2009;297(1):H153–62.CrossRefPubMed
37.
Zurück zum Zitat Frustaci A, Kajstura J, Chimenti C, Jakoniuk I, Leri A, Maseri A, et al. Myocardial cell death in human diabetes. Circ Res. 2000;87(12):1123–32.PubMed Frustaci A, Kajstura J, Chimenti C, Jakoniuk I, Leri A, Maseri A, et al. Myocardial cell death in human diabetes. Circ Res. 2000;87(12):1123–32.PubMed
38.
Zurück zum Zitat Aragno M, Mastrocola R, Medana C, Catalano MG, Vercellinatto I, Danni O, et al. Oxidative stress-dependent impairment of cardiac-specific transcription factors in experimental diabetes. Endocrinology 2006;147(12):5967–74.CrossRefPubMed Aragno M, Mastrocola R, Medana C, Catalano MG, Vercellinatto I, Danni O, et al. Oxidative stress-dependent impairment of cardiac-specific transcription factors in experimental diabetes. Endocrinology 2006;147(12):5967–74.CrossRefPubMed
39.
Zurück zum Zitat Chowdhry MF, Vohra HA, Galinanes M. Diabetes increases apoptosis and necrosis in both ischemic and nonischemic human myocardium: role of caspases and poly-adenosine diphosphate-ribose polymerase. J Thorac Cardiovasc Surg. 2007;134(1):124–31. 131 e121–123.CrossRefPubMed Chowdhry MF, Vohra HA, Galinanes M. Diabetes increases apoptosis and necrosis in both ischemic and nonischemic human myocardium: role of caspases and poly-adenosine diphosphate-ribose polymerase. J Thorac Cardiovasc Surg. 2007;134(1):124–31. 131 e121–123.CrossRefPubMed
40.
Zurück zum Zitat Barouch LA, Gao D, Chen L, Miller KL, Xu W, Phan AC, et al. Cardiac myocyte apoptosis is associated with increased DNA damage and decreased survival in murine models of obesity. Circ Res. 2006;98(1):119–24.CrossRefPubMed Barouch LA, Gao D, Chen L, Miller KL, Xu W, Phan AC, et al. Cardiac myocyte apoptosis is associated with increased DNA damage and decreased survival in murine models of obesity. Circ Res. 2006;98(1):119–24.CrossRefPubMed
41.
Zurück zum Zitat Shen E, Li Y, Shan L, Zhu H, Feng Q, Arnold JM, et al. Rac1 is required for cardiomyocyte apoptosis during hyperglycemia. Diabetes 2009;58(10):2386–95.CrossRefPubMed Shen E, Li Y, Shan L, Zhu H, Feng Q, Arnold JM, et al. Rac1 is required for cardiomyocyte apoptosis during hyperglycemia. Diabetes 2009;58(10):2386–95.CrossRefPubMed
42.
Zurück zum Zitat Dhalla NS, Liu X, Panagia V, Takeda N. Subcellular remodeling and heart dysfunction in chronic diabetes. Cardiovasc Res. 1998;40(2):239–47.CrossRefPubMed Dhalla NS, Liu X, Panagia V, Takeda N. Subcellular remodeling and heart dysfunction in chronic diabetes. Cardiovasc Res. 1998;40(2):239–47.CrossRefPubMed
43.
Zurück zum Zitat Brenner BM, Cooper ME, de Zeeuw D, Keane WF, Mitch WE, Parving HH, et al. Effects of losartan on renal and cardiovascular outcomes in patients with type 2 diabetes and nephropathy. N Engl J Med. 2001;345(12):861–9.CrossRefPubMed Brenner BM, Cooper ME, de Zeeuw D, Keane WF, Mitch WE, Parving HH, et al. Effects of losartan on renal and cardiovascular outcomes in patients with type 2 diabetes and nephropathy. N Engl J Med. 2001;345(12):861–9.CrossRefPubMed
44.
Zurück zum Zitat Symeonides P, Koulouris S, Vratsista E, Triantafyllou K, Ioannidis G, Thalassinos N, et al. Both ramipril and telmisartan reverse indices of early diabetic cardiomyopathy: a comparative study. Eur J Echocardiog. 2007;8(6):480–6.CrossRef Symeonides P, Koulouris S, Vratsista E, Triantafyllou K, Ioannidis G, Thalassinos N, et al. Both ramipril and telmisartan reverse indices of early diabetic cardiomyopathy: a comparative study. Eur J Echocardiog. 2007;8(6):480–6.CrossRef
45.
Zurück zum Zitat Tsutsui H, Matsushima S, Kinugawa S, Ide T, Inoue N, Ohta Y, et al. Angiotensin II type 1 receptor blocker attenuates myocardial remodeling and preserves diastolic function in diabetic heart. Hypertens Res. 2007;30(5):439–49.CrossRefPubMed Tsutsui H, Matsushima S, Kinugawa S, Ide T, Inoue N, Ohta Y, et al. Angiotensin II type 1 receptor blocker attenuates myocardial remodeling and preserves diastolic function in diabetic heart. Hypertens Res. 2007;30(5):439–49.CrossRefPubMed
46.
Zurück zum Zitat Shimizu M, Umeda K, Sugihara N, Yoshio H, Ino H, Takeda R, et al. Collagen remodelling in myocardia of patients with diabetes. J Clin Pathol. 1993;46(1):32–6.CrossRefPubMed Shimizu M, Umeda K, Sugihara N, Yoshio H, Ino H, Takeda R, et al. Collagen remodelling in myocardia of patients with diabetes. J Clin Pathol. 1993;46(1):32–6.CrossRefPubMed
47.
Zurück zum Zitat Gonzalez-Vilchez F, Ayuela J, Ares M, Pi J, Castillo L, Martin-Duran R. Oxidative stress and fibrosis in incipient myocardial dysfunction in type 2 diabetic patients. Int J Cardiol. 2005;101(1):53–8.CrossRefPubMed Gonzalez-Vilchez F, Ayuela J, Ares M, Pi J, Castillo L, Martin-Duran R. Oxidative stress and fibrosis in incipient myocardial dysfunction in type 2 diabetic patients. Int J Cardiol. 2005;101(1):53–8.CrossRefPubMed
48.
Zurück zum Zitat Ihm SH, Youn HJ, Shin DI, Jang SW, Park CS, Kim PJ, et al. Serum carboxy-terminal propeptide of type I procollagen (PIP) is a marker of diastolic dysfunction in patients with early type 2 diabetes mellitus. Int J Cardiol. 2007;122(3):e36–8.PubMed Ihm SH, Youn HJ, Shin DI, Jang SW, Park CS, Kim PJ, et al. Serum carboxy-terminal propeptide of type I procollagen (PIP) is a marker of diastolic dysfunction in patients with early type 2 diabetes mellitus. Int J Cardiol. 2007;122(3):e36–8.PubMed
49.
Zurück zum Zitat Mizushige K, Yao L, Noma T, Kiyomoto H, Yu Y, Hosomi N, et al. Alteration in left ventricular diastolic filling and accumulation of myocardial collagen at insulin-resistant prediabetic stage of a type II diabetic rat model. Circulation 2000;101(8):899–907.PubMed Mizushige K, Yao L, Noma T, Kiyomoto H, Yu Y, Hosomi N, et al. Alteration in left ventricular diastolic filling and accumulation of myocardial collagen at insulin-resistant prediabetic stage of a type II diabetic rat model. Circulation 2000;101(8):899–907.PubMed
50.
Zurück zum Zitat Ban CR, Twigg SM. Fibrosis in diabetes complications: pathogenic mechanisms and circulating and urinary markers. Vasc Health Risk Manag. 2008;4(3):575–96.PubMed Ban CR, Twigg SM. Fibrosis in diabetes complications: pathogenic mechanisms and circulating and urinary markers. Vasc Health Risk Manag. 2008;4(3):575–96.PubMed
51.
Zurück zum Zitat Way KJ, Isshiki K, Suzuma K, Yokota T, Zvagelsky D, Schoen FJ, et al. Expression of connective tissue growth factor is increased in injured myocardium associated with protein kinase C beta2 activation and diabetes. Diabetes 2002;51(9):2709–18.CrossRefPubMed Way KJ, Isshiki K, Suzuma K, Yokota T, Zvagelsky D, Schoen FJ, et al. Expression of connective tissue growth factor is increased in injured myocardium associated with protein kinase C beta2 activation and diabetes. Diabetes 2002;51(9):2709–18.CrossRefPubMed
52.
Zurück zum Zitat McQueen AP, Zhang D, Hu P, Swenson L, Yang Y, Zaha VG, et al. Contractile dysfunction in hypertrophied hearts with deficient insulin receptor signaling: possible role of reduced capillary density. J Mol Cell Cardiol. 2005;39(6):882–92.CrossRefPubMed McQueen AP, Zhang D, Hu P, Swenson L, Yang Y, Zaha VG, et al. Contractile dysfunction in hypertrophied hearts with deficient insulin receptor signaling: possible role of reduced capillary density. J Mol Cell Cardiol. 2005;39(6):882–92.CrossRefPubMed
53.
Zurück zum Zitat Van den Bergh A, Vanderper A, Vangheluwe P, Desjardins F, Nevelsteen I, Verreth W, et al. Dyslipidaemia in type II diabetic mice does not aggravate contractile impairment but increases ventricular stiffness. Cardiovasc Res. 2008;77(2):371–9.CrossRefPubMed Van den Bergh A, Vanderper A, Vangheluwe P, Desjardins F, Nevelsteen I, Verreth W, et al. Dyslipidaemia in type II diabetic mice does not aggravate contractile impairment but increases ventricular stiffness. Cardiovasc Res. 2008;77(2):371–9.CrossRefPubMed
54.
Zurück zum Zitat Brooks BA, Franjic B, Ban CR, Swaraj K, Yue DK, Celermajer DS, et al. Diastolic dysfunction and abnormalities of the microcirculation in type 2 diabetes. Diabetes Obes Metab. 2008;10(9):739–46.CrossRefPubMed Brooks BA, Franjic B, Ban CR, Swaraj K, Yue DK, Celermajer DS, et al. Diastolic dysfunction and abnormalities of the microcirculation in type 2 diabetes. Diabetes Obes Metab. 2008;10(9):739–46.CrossRefPubMed
55.
Zurück zum Zitat Shivalkar B, Dhondt D, Goovaerts I, Van Gaal L, Bartunek J, Van Crombrugge P, et al. Flow mediated dilatation and cardiac function in type 1 diabetes mellitus. Am J Cardiol. 2006;97(1):77–82.CrossRefPubMed Shivalkar B, Dhondt D, Goovaerts I, Van Gaal L, Bartunek J, Van Crombrugge P, et al. Flow mediated dilatation and cardiac function in type 1 diabetes mellitus. Am J Cardiol. 2006;97(1):77–82.CrossRefPubMed
56.
Zurück zum Zitat Ozasa N, Furukawa Y, Morimoto T, Tadamura E, Kita T, Kimura T. Relation among left ventricular mass, insulin resistance, and hemodynamic parameters in type 2 diabetes. Hypertens Res. 2008;31(3):425–32.CrossRefPubMed Ozasa N, Furukawa Y, Morimoto T, Tadamura E, Kita T, Kimura T. Relation among left ventricular mass, insulin resistance, and hemodynamic parameters in type 2 diabetes. Hypertens Res. 2008;31(3):425–32.CrossRefPubMed
57.
Zurück zum Zitat Hsueh W, Abel ED, Breslow JL, Maeda N, Davis RC, Fisher EA, et al. Recipes for creating animal models of diabetic cardiovascular disease. Circ Res. 2007;100(10):1415–27.CrossRefPubMed Hsueh W, Abel ED, Breslow JL, Maeda N, Davis RC, Fisher EA, et al. Recipes for creating animal models of diabetic cardiovascular disease. Circ Res. 2007;100(10):1415–27.CrossRefPubMed
58.
Zurück zum Zitat Russell JC, Proctor SD. Small animal models of cardiovascular disease: tools for the study of the roles of metabolic syndrome, dyslipidemia, and atherosclerosis. Cardiovasc Pathol. 2006;15(6):318–30.CrossRefPubMed Russell JC, Proctor SD. Small animal models of cardiovascular disease: tools for the study of the roles of metabolic syndrome, dyslipidemia, and atherosclerosis. Cardiovasc Pathol. 2006;15(6):318–30.CrossRefPubMed
59.
Zurück zum Zitat Semeniuk LM, Kryski AJ, Severson DL. Echocardiographic assessment of cardiac function in diabetic db/db and transgenic db/db-hGLUT4 mice. Am J Physiol Heart Circ Physiol. 2002;283(3):H976–82.PubMed Semeniuk LM, Kryski AJ, Severson DL. Echocardiographic assessment of cardiac function in diabetic db/db and transgenic db/db-hGLUT4 mice. Am J Physiol Heart Circ Physiol. 2002;283(3):H976–82.PubMed
60.
Zurück zum Zitat Aasum E, Belke DD, Severson DL, Riemersma RA, Cooper M, Andreassen M, et al. Cardiac function and metabolism in Type 2 diabetic mice after treatment with BM 17.0744, a novel PPAR-alpha activator. Am J Physiol Heart Circ Physiol. 2002;283(3):H949–57.PubMed Aasum E, Belke DD, Severson DL, Riemersma RA, Cooper M, Andreassen M, et al. Cardiac function and metabolism in Type 2 diabetic mice after treatment with BM 17.0744, a novel PPAR-alpha activator. Am J Physiol Heart Circ Physiol. 2002;283(3):H949–57.PubMed
61.
Zurück zum Zitat Aasum E, Hafstad AD, Severson DL, Larsen TS. Age-dependent changes in metabolism, contractile function, and ischemic sensitivity in hearts from db/db mice. Diabetes 2003;52(2):434–41.CrossRefPubMed Aasum E, Hafstad AD, Severson DL, Larsen TS. Age-dependent changes in metabolism, contractile function, and ischemic sensitivity in hearts from db/db mice. Diabetes 2003;52(2):434–41.CrossRefPubMed
62.
Zurück zum Zitat Christoffersen C, Bollano E, Lindegaard ML, Bartels ED, Goetze JP, Andersen CB, et al. Cardiac lipid accumulation associated with diastolic dysfunction in obese mice. Endocrinology 2003;144(8):3483–90.CrossRefPubMed Christoffersen C, Bollano E, Lindegaard ML, Bartels ED, Goetze JP, Andersen CB, et al. Cardiac lipid accumulation associated with diastolic dysfunction in obese mice. Endocrinology 2003;144(8):3483–90.CrossRefPubMed
63.
Zurück zum Zitat Dong F, Zhang X, Yang X, Esberg LB, Yang H, Zhang Z, et al. Impaired cardiac contractile function in ventricular myocytes from leptin-deficient ob/ob obese mice. J Endocrinol. 2006;188(1):25–36.CrossRefPubMed Dong F, Zhang X, Yang X, Esberg LB, Yang H, Zhang Z, et al. Impaired cardiac contractile function in ventricular myocytes from leptin-deficient ob/ob obese mice. J Endocrinol. 2006;188(1):25–36.CrossRefPubMed
64.
Zurück zum Zitat Stolen TO, Hoydal MA, Kemi OJ, Catalucci D, Ceci M, Aasum E, et al. Interval training normalizes cardiomyocyte function, diastolic Ca2+ control, and SR Ca2+ release synchronicity in a mouse model of diabetic cardiomyopathy. Circ Res. 2009;105(6):527–36.CrossRefPubMed Stolen TO, Hoydal MA, Kemi OJ, Catalucci D, Ceci M, Aasum E, et al. Interval training normalizes cardiomyocyte function, diastolic Ca2+ control, and SR Ca2+ release synchronicity in a mouse model of diabetic cardiomyopathy. Circ Res. 2009;105(6):527–36.CrossRefPubMed
65.
Zurück zum Zitat Fang ZY, Schull-Meade R, Leano R, Mottram PM, Prins JB, Marwick TH. Screening for heart disease in diabetic subjects. Am Heart J. 2005;149(2):349–54.CrossRefPubMed Fang ZY, Schull-Meade R, Leano R, Mottram PM, Prins JB, Marwick TH. Screening for heart disease in diabetic subjects. Am Heart J. 2005;149(2):349–54.CrossRefPubMed
66.
Zurück zum Zitat Yu CM, Chau E, Sanderson JE, Fan K, Tang MO, Fung WH, et al. Tissue Doppler echocardiographic evidence of reverse remodeling and improved synchronicity by simultaneously delaying regional contraction after biventricular pacing therapy in heart failure. Circulation 2002;105(4):438–45.CrossRefPubMed Yu CM, Chau E, Sanderson JE, Fan K, Tang MO, Fung WH, et al. Tissue Doppler echocardiographic evidence of reverse remodeling and improved synchronicity by simultaneously delaying regional contraction after biventricular pacing therapy in heart failure. Circulation 2002;105(4):438–45.CrossRefPubMed
67.
Zurück zum Zitat Yue P, Arai T, Terashima M, Sheikh AY, Cao F, Charo D, et al. Magnetic resonance imaging of progressive cardiomyopathic changes in the db/db mouse. Am J Physiol Heart Circ Physiol. 2007;292(5):H2106–18.CrossRefPubMed Yue P, Arai T, Terashima M, Sheikh AY, Cao F, Charo D, et al. Magnetic resonance imaging of progressive cardiomyopathic changes in the db/db mouse. Am J Physiol Heart Circ Physiol. 2007;292(5):H2106–18.CrossRefPubMed
68.
Zurück zum Zitat Van den Bergh A, Flameng W, Herijgers P. Type II diabetic mice exhibit contractile dysfunction but maintain cardiac output by favourable loading conditions. Eur J Heart Fail. 2006;8(8):777–83.CrossRefPubMed Van den Bergh A, Flameng W, Herijgers P. Type II diabetic mice exhibit contractile dysfunction but maintain cardiac output by favourable loading conditions. Eur J Heart Fail. 2006;8(8):777–83.CrossRefPubMed
69.
Zurück zum Zitat Radovits T, Korkmaz S, Loganathan S, Barnucz E, Bomicke T, Arif R, et al. Comparative investigation of the left ventricular pressure-volume relationship in rat models of type 1 and type 2 diabetes mellitus. Am J Physiol Heart Circ Physiol. 2009;297(1):H125–33.CrossRefPubMed Radovits T, Korkmaz S, Loganathan S, Barnucz E, Bomicke T, Arif R, et al. Comparative investigation of the left ventricular pressure-volume relationship in rat models of type 1 and type 2 diabetes mellitus. Am J Physiol Heart Circ Physiol. 2009;297(1):H125–33.CrossRefPubMed
70.
Zurück zum Zitat Scognamiglio R, Avogaro A, Casara D, Crepaldi C, Marin M, Palisi M, et al. Myocardial dysfunction and adrenergic cardiac innervation in patients with insulin-dependent diabetes mellitus. J Am Coll Cardiol. 1998;31(2):404–12.CrossRefPubMed Scognamiglio R, Avogaro A, Casara D, Crepaldi C, Marin M, Palisi M, et al. Myocardial dysfunction and adrenergic cardiac innervation in patients with insulin-dependent diabetes mellitus. J Am Coll Cardiol. 1998;31(2):404–12.CrossRefPubMed
71.
Zurück zum Zitat Ha JW, Lee HC, Kang ES, Ahn CM, Kim JM, Ahn JA, et al. Abnormal left ventricular longitudinal functional reserve in patients with diabetes mellitus: implication for detecting subclinical myocardial dysfunction using exercise tissue Doppler echocardiography. Heart 2007;93(12):1571–6.CrossRefPubMed Ha JW, Lee HC, Kang ES, Ahn CM, Kim JM, Ahn JA, et al. Abnormal left ventricular longitudinal functional reserve in patients with diabetes mellitus: implication for detecting subclinical myocardial dysfunction using exercise tissue Doppler echocardiography. Heart 2007;93(12):1571–6.CrossRefPubMed
72.
Zurück zum Zitat Palmieri V, Capaldo B, Russo C, Iaccarino M, Pezzullo S, Quintavalle G, et al. Uncomplicated type 1 diabetes and preclinical left ventricular myocardial dysfunction: insights from echocardiography and exercise cardiac performance evaluation. Diabetes Res Clin Pract. 2008;79(2):262–8.CrossRefPubMed Palmieri V, Capaldo B, Russo C, Iaccarino M, Pezzullo S, Quintavalle G, et al. Uncomplicated type 1 diabetes and preclinical left ventricular myocardial dysfunction: insights from echocardiography and exercise cardiac performance evaluation. Diabetes Res Clin Pract. 2008;79(2):262–8.CrossRefPubMed
73.
Zurück zum Zitat Abe T, Ohga Y, Tabayashi N, Kobayashi S, Sakata S, Misawa H, et al. Left ventricular diastolic dysfunction in type 2 diabetes mellitus model rats. Am J Physiol Heart Circ Physiol. 2002;282(1):H138–48.PubMed Abe T, Ohga Y, Tabayashi N, Kobayashi S, Sakata S, Misawa H, et al. Left ventricular diastolic dysfunction in type 2 diabetes mellitus model rats. Am J Physiol Heart Circ Physiol. 2002;282(1):H138–48.PubMed
74.
Zurück zum Zitat 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(17):2686–95.CrossRefPubMed 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(17):2686–95.CrossRefPubMed
75.
Zurück zum Zitat Bugger H, Abel ED. Rodent models of diabetic cardiomyopathy. Dis Model Mech. 2009;2(9–10):454–66.CrossRefPubMed Bugger H, Abel ED. Rodent models of diabetic cardiomyopathy. Dis Model Mech. 2009;2(9–10):454–66.CrossRefPubMed
76.
Zurück zum Zitat Joshi D, Gupta R, Dubey A, Shiwalkar A, Pathak P, Gupta RC, et al. TRC4186, a novel AGE-breaker, improves diabetic cardiomyopathy and nephropathy in Ob-ZSF1 model of type 2 diabetes. J Cardiovasc Pharmacol. 2009;54(1):72–81.CrossRefPubMed Joshi D, Gupta R, Dubey A, Shiwalkar A, Pathak P, Gupta RC, et al. TRC4186, a novel AGE-breaker, improves diabetic cardiomyopathy and nephropathy in Ob-ZSF1 model of type 2 diabetes. J Cardiovasc Pharmacol. 2009;54(1):72–81.CrossRefPubMed
77.
Zurück zum Zitat Lamounier-Zepter V, Look C, Alvarez J, Christ T, Ravens U, Schunck WH, et al. Adipocyte fatty acid-binding protein suppresses cardiomyocyte contraction: a new link between obesity and heart disease. Circ Res. 2009;105(4):326–34.CrossRefPubMed Lamounier-Zepter V, Look C, Alvarez J, Christ T, Ravens U, Schunck WH, et al. Adipocyte fatty acid-binding protein suppresses cardiomyocyte contraction: a new link between obesity and heart disease. Circ Res. 2009;105(4):326–34.CrossRefPubMed
78.
Zurück zum Zitat Bugger H, Abel ED. Molecular mechanisms for myocardial mitochondrial dysfunction in the metabolic syndrome. Clin Sci (Lond) 2008;114(3):195–210.CrossRef Bugger H, Abel ED. Molecular mechanisms for myocardial mitochondrial dysfunction in the metabolic syndrome. Clin Sci (Lond) 2008;114(3):195–210.CrossRef
79.
Zurück zum Zitat Wright JJ, Kim J, Buchanan J, Boudina S, Sena S, Bakirtzi K, et al. Mechanisms for increased myocardial fatty acid utilization following short-term high-fat feeding. Cardiovasc Res. 2009;82(2):351–60.CrossRefPubMed Wright JJ, Kim J, Buchanan J, Boudina S, Sena S, Bakirtzi K, et al. Mechanisms for increased myocardial fatty acid utilization following short-term high-fat feeding. Cardiovasc Res. 2009;82(2):351–60.CrossRefPubMed
80.
Zurück zum Zitat Buchanan J, Mazumder PK, Hu P, Chakrabarti G, Roberts MW, Yun UJ, 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(12):5341–9.CrossRefPubMed Buchanan J, Mazumder PK, Hu P, Chakrabarti G, Roberts MW, Yun UJ, 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(12):5341–9.CrossRefPubMed
81.
Zurück zum Zitat Thai MV, Guruswamy S, Cao KT, Pessin JE, Olson AL. Myocyte enhancer factor 2 (MEF2)-binding site is required for GLUT4 gene expression in transgenic mice. Regulation of MEF2 DNA binding activity in insulin-deficient diabetes. J Biol Chem. 1998;273(23):14285–92.CrossRefPubMed Thai MV, Guruswamy S, Cao KT, Pessin JE, Olson AL. Myocyte enhancer factor 2 (MEF2)-binding site is required for GLUT4 gene expression in transgenic mice. Regulation of MEF2 DNA binding activity in insulin-deficient diabetes. J Biol Chem. 1998;273(23):14285–92.CrossRefPubMed
82.
Zurück zum Zitat Razeghi P, Young ME, Cockrill TC, Frazier OH, Taegtmeyer H. Downregulation of myocardial myocyte enhancer factor 2C and myocyte enhancer factor 2C-regulated gene expression in diabetic patients with nonischemic heart failure. Circulation 2002;106(4):407–11.CrossRefPubMed Razeghi P, Young ME, Cockrill TC, Frazier OH, Taegtmeyer H. Downregulation of myocardial myocyte enhancer factor 2C and myocyte enhancer factor 2C-regulated gene expression in diabetic patients with nonischemic heart failure. Circulation 2002;106(4):407–11.CrossRefPubMed
83.
Zurück zum Zitat How OJ, Aasum E, Severson DL, Chan WY, Essop MF, Larsen TS. Increased myocardial oxygen consumption reduces cardiac efficiency in diabetic mice. Diabetes 2006;55(2):466–73.CrossRefPubMed How OJ, Aasum E, Severson DL, Chan WY, Essop MF, Larsen TS. Increased myocardial oxygen consumption reduces cardiac efficiency in diabetic mice. Diabetes 2006;55(2):466–73.CrossRefPubMed
84.
Zurück zum Zitat Mazumder PK, O’Neill BT, Roberts MW, Buchanan J, Yun UJ, Cooksey RC, et al. Impaired cardiac efficiency and increased fatty acid oxidation in insulin-resistant ob/ob mouse hearts. Diabetes 2004;53(9):2366–74.CrossRefPubMed Mazumder PK, O’Neill BT, Roberts MW, Buchanan J, Yun UJ, Cooksey RC, et al. Impaired cardiac efficiency and increased fatty acid oxidation in insulin-resistant ob/ob mouse hearts. Diabetes 2004;53(9):2366–74.CrossRefPubMed
85.
Zurück zum Zitat Peterson LR, Herrero P, McGill J, Schechtman KB, Kisrieva-Ware Z, Lesniak D, et al. Fatty acids and insulin modulate myocardial substrate metabolism in humans with type 1 diabetes. Diabetes 2008;57(1):32–40.CrossRefPubMed Peterson LR, Herrero P, McGill J, Schechtman KB, Kisrieva-Ware Z, Lesniak D, et al. Fatty acids and insulin modulate myocardial substrate metabolism in humans with type 1 diabetes. Diabetes 2008;57(1):32–40.CrossRefPubMed
86.
Zurück zum Zitat Peterson LR, Herrero P, Schechtman KB, Racette SB, Waggoner AD, Kisrieva-Ware Z, et al. Effect of obesity and insulin resistance on myocardial substrate metabolism and efficiency in young women. Circulation 2004;109(18):2191–6.CrossRefPubMed Peterson LR, Herrero P, Schechtman KB, Racette SB, Waggoner AD, Kisrieva-Ware Z, et al. Effect of obesity and insulin resistance on myocardial substrate metabolism and efficiency in young women. Circulation 2004;109(18):2191–6.CrossRefPubMed
87.
Zurück zum Zitat Boudina S, Abel ED. Mitochondrial uncoupling: a key contributor to reduced cardiac efficiency in diabetes. Physiology (Bethesda) 2006;21:250–8. Boudina S, Abel ED. Mitochondrial uncoupling: a key contributor to reduced cardiac efficiency in diabetes. Physiology (Bethesda) 2006;21:250–8.
88.
Zurück zum Zitat Bugger H, Chen D, Riehle C, Soto J, Theobald HA, Hu XX, et al. Tissue-specific remodeling of the mitochondrial proteome in type 1 diabetic akita mice. Diabetes 2009;58(9):1986–97.CrossRefPubMed Bugger H, Chen D, Riehle C, Soto J, Theobald HA, Hu XX, et al. Tissue-specific remodeling of the mitochondrial proteome in type 1 diabetic akita mice. Diabetes 2009;58(9):1986–97.CrossRefPubMed
89.
Zurück zum Zitat Diamant M, Lamb HJ, Groeneveld Y, Endert EL, Smit JW, Bax JJ, et al. Diastolic dysfunction is associated with altered myocardial metabolism in asymptomatic normotensive patients with well-controlled type 2 diabetes mellitus. J Am Coll Cardiol. 2003;42(2):328–35.CrossRefPubMed Diamant M, Lamb HJ, Groeneveld Y, Endert EL, Smit JW, Bax JJ, et al. Diastolic dysfunction is associated with altered myocardial metabolism in asymptomatic normotensive patients with well-controlled type 2 diabetes mellitus. J Am Coll Cardiol. 2003;42(2):328–35.CrossRefPubMed
90.
Zurück zum Zitat Metzler B, Schocke MF, Steinboeck P, Wolf C, Judmaier W, Lechleitner M, et al. Decreased high-energy phosphate ratios in the myocardium of men with diabetes mellitus type I. J Cardiovasc Magn Reson. 2002;4(4):493–502.CrossRefPubMed Metzler B, Schocke MF, Steinboeck P, Wolf C, Judmaier W, Lechleitner M, et al. Decreased high-energy phosphate ratios in the myocardium of men with diabetes mellitus type I. J Cardiovasc Magn Reson. 2002;4(4):493–502.CrossRefPubMed
91.
Zurück zum Zitat Scheuermann-Freestone M, Madsen PL, Manners D, Blamire AM, Buckingham RE, Styles P, et al. Abnormal cardiac and skeletal muscle energy metabolism in patients with type 2 diabetes. Circulation 2003;107(24):3040–6.CrossRefPubMed Scheuermann-Freestone M, Madsen PL, Manners D, Blamire AM, Buckingham RE, Styles P, et al. Abnormal cardiac and skeletal muscle energy metabolism in patients with type 2 diabetes. Circulation 2003;107(24):3040–6.CrossRefPubMed
92.
Zurück zum Zitat Rijzewijk LJ, van der Meer RW, Lamb HJ, de Jong HW, Lubberink M, Romijn JA, et al. Altered myocardial substrate metabolism and decreased diastolic function in nonischemic human diabetic cardiomyopathy: studies with cardiac positron emission tomography and magnetic resonance imaging. J Am Coll Cardiol. 2009;54(16):1524–32.CrossRefPubMed Rijzewijk LJ, van der Meer RW, Lamb HJ, de Jong HW, Lubberink M, Romijn JA, et al. Altered myocardial substrate metabolism and decreased diastolic function in nonischemic human diabetic cardiomyopathy: studies with cardiac positron emission tomography and magnetic resonance imaging. J Am Coll Cardiol. 2009;54(16):1524–32.CrossRefPubMed
93.
Zurück zum Zitat Anderson EJ, Kypson AP, Rodriguez E, Anderson CA, Lehr EJ, Neufer PD. Substrate-specific derangements in mitochondrial metabolism and redox balance in the atrium of the type 2 diabetic human heart. J Am Coll Cardiol. 2009;54(20):1891–8.CrossRefPubMed Anderson EJ, Kypson AP, Rodriguez E, Anderson CA, Lehr EJ, Neufer PD. Substrate-specific derangements in mitochondrial metabolism and redox balance in the atrium of the type 2 diabetic human heart. J Am Coll Cardiol. 2009;54(20):1891–8.CrossRefPubMed
94.
Zurück zum Zitat Hassouna A, Loubani M, Matata BM, Fowler A, Standen NB, Galinanes M. Mitochondrial dysfunction as the cause of the failure to precondition the diabetic human myocardium. Cardiovasc Res. 2006;69(2):450–8.CrossRefPubMed Hassouna A, Loubani M, Matata BM, Fowler A, Standen NB, Galinanes M. Mitochondrial dysfunction as the cause of the failure to precondition the diabetic human myocardium. Cardiovasc Res. 2006;69(2):450–8.CrossRefPubMed
95.
Zurück zum Zitat Echtay KS, Esteves TC, Pakay JL, Jekabsons MB, Lambert AJ, Portero-Otin M, et al. A signalling role for 4-hydroxy-2-nonenal in regulation of mitochondrial uncoupling. EMBO J. 2003;22(16):4103–10.CrossRefPubMed Echtay KS, Esteves TC, Pakay JL, Jekabsons MB, Lambert AJ, Portero-Otin M, et al. A signalling role for 4-hydroxy-2-nonenal in regulation of mitochondrial uncoupling. EMBO J. 2003;22(16):4103–10.CrossRefPubMed
96.
Zurück zum Zitat Herlein JA, Fink BD, O’Malley Y, Sivitz WI. Superoxide and respiratory coupling in mitochondria of insulin-deficient diabetic rats. Endocrinology 2009;150(1):46–55.CrossRefPubMed Herlein JA, Fink BD, O’Malley Y, Sivitz WI. Superoxide and respiratory coupling in mitochondria of insulin-deficient diabetic rats. Endocrinology 2009;150(1):46–55.CrossRefPubMed
Metadaten
Titel
Diabetic cardiomyopathy, causes and effects
verfasst von
Sihem Boudina
Evan Dale Abel
Publikationsdatum
01.03.2010
Verlag
Springer US
Erschienen in
Reviews in Endocrine and Metabolic Disorders / Ausgabe 1/2010
Print ISSN: 1389-9155
Elektronische ISSN: 1573-2606
DOI
https://doi.org/10.1007/s11154-010-9131-7

Weitere Artikel der Ausgabe 1/2010

Reviews in Endocrine and Metabolic Disorders 1/2010 Zur Ausgabe

Leitlinien kompakt für die Innere Medizin

Mit medbee Pocketcards sicher entscheiden.

Seit 2022 gehört die medbee GmbH zum Springer Medizin Verlag

Mehr Lebenszeit mit Abemaciclib bei fortgeschrittenem Brustkrebs?

24.05.2024 Mammakarzinom Nachrichten

In der MONARCHE-3-Studie lebten Frauen mit fortgeschrittenem Hormonrezeptor-positivem, HER2-negativem Brustkrebs länger, wenn sie zusätzlich zu einem nicht steroidalen Aromatasehemmer mit Abemaciclib behandelt wurden; allerdings verfehlte der numerische Zugewinn die statistische Signifikanz.

ADT zur Radiatio nach Prostatektomie: Wenn, dann wohl länger

24.05.2024 Prostatakarzinom Nachrichten

Welchen Nutzen es trägt, wenn die Strahlentherapie nach radikaler Prostatektomie um eine Androgendeprivation ergänzt wird, hat die RADICALS-HD-Studie untersucht. Nun liegen die Ergebnisse vor. Sie sprechen für länger dauernden Hormonentzug.

„Überwältigende“ Evidenz für Tripeltherapie beim metastasierten Prostata-Ca.

22.05.2024 Prostatakarzinom Nachrichten

Patienten mit metastasiertem hormonsensitivem Prostatakarzinom sollten nicht mehr mit einer alleinigen Androgendeprivationstherapie (ADT) behandelt werden, mahnt ein US-Team nach Sichtung der aktuellen Datenlage. Mit einer Tripeltherapie haben die Betroffenen offenbar die besten Überlebenschancen.

So sicher sind Tattoos: Neue Daten zur Risikobewertung

22.05.2024 Melanom Nachrichten

Das größte medizinische Problem bei Tattoos bleiben allergische Reaktionen. Melanome werden dadurch offensichtlich nicht gefördert, die Farbpigmente könnten aber andere Tumoren begünstigen.

Update Innere Medizin

Bestellen Sie unseren Fach-Newsletter und bleiben Sie gut informiert.