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Metabolic and Contractile Remodelling in the Diabetic Heart: An Evolutionary Perspective

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Diabetic Cardiomyopathy

Part of the book series: Advances in Biochemistry in Health and Disease ((ABHD,volume 9))

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Abstract

The application of evolutionary biology to the study of human disease has given rise to the idea that disease can result from inappropriate adaptations to a change in environment. This concept can also be applied to the function of organs and responding to their local environments within the human body. The heart is an omnivorous organ which can use any substrate it is supplied with. The metabolic machinery of the heart is exquisitely attuned both to its metabolic needs and to the available energy substrates in its local environment. Diabetic cardiomyopathy is a disease process which arises as a result of the inability of the heart to adapt to a diabetic metabolic milieu. The heart becomes locked into a progressively maladaptive state from which it cannot escape by its own devices; due to the phenomenon of hyperglycemic memory, even restoration of a normal milieu may not be sufficient to completely reverse the remodeling. The pathways which initiate, progress and perpetuate this downward spiral are the same pathways which normally allow the heart to sense and respond to its local metabolic environment. These include metabolite-sensitive transcriptional regulatory pathways and, most probably, epigenetic and miRNA regulatory pathways. Overall, the application of evolutionary concepts provides a valuable framework for understanding the origins and importance of metabolic and contractile disturbances in the diabetic heart, and a strong rationale for the use of metabolic therapy as a treatment.

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References

  1. Bishopric NH (2005) Evolution of the heart from bacteria to man. Ann N Y Acad Sci 1047: 13–29

    Article  CAS  PubMed  Google Scholar 

  2. Stanley WC, Chandler MP (2002) Energy metabolism in the normal and failing heart: potential for therapeutic interventions. Heart Fail Rev 7:115–130

    Article  CAS  PubMed  Google Scholar 

  3. Driedzic WR, Sidell BD, Stowe D et al (1987) Matching of vertebrate cardiac energy demand to energy metabolism. Am J Physiol 252:R930–R937

    CAS  PubMed  Google Scholar 

  4. Clark AJ, Gaddie R, Stewart CP (1932) The carbohydrate metabolism of the isolated heart of the frog. J Physiol 75:311–320

    CAS  PubMed  Google Scholar 

  5. Neely JR, Morgan HE (1974) Relationship between carbohydrate metabolism and energy balance of heart muscle. Annu Rev Physiol 36:413–459

    Article  CAS  PubMed  Google Scholar 

  6. Sidell BD, Stowe DB, Hansen CA (1984) Carbohydrate is the preferred metabolic fuel of the hagfish (Myxine glutinosa) heart. Physiol Zool 7:266–273

    Google Scholar 

  7. Moyes CD (1996) Cardiac metabolism in high performance fish. Comp Biochem Physiol 113A:69–75

    Article  CAS  Google Scholar 

  8. Wu JJ, Chang I (1948) The glycolytic activity of the hearts of vertebrates. Q J Exp Physiol Cogn Med Sci 34:91–95

    CAS  PubMed  Google Scholar 

  9. Moyes CD, Suarez RK, Hochachka PW (1989) A comparison of fuel preferences of mitochondria from vertebrates and invertebrates. Can J Zool/Rev Can Zool 68:1337–1349

    Article  Google Scholar 

  10. Beall CM (2007) Detecting natural selection in high-altitude human populations. Respir Physiol Neurobiol 158:161–171

    Article  PubMed  Google Scholar 

  11. Moore LG (2001) Human genetic adaptation to high altitude. High Alt Med Biol 2:257–279

    Article  CAS  PubMed  Google Scholar 

  12. Rupert JL, Hochachka PW (2001) The evidence for hereditary factors contributing to high altitude adaptation in Andean natives: a review. High Alt Med Biol 2:235–256

    Article  CAS  PubMed  Google Scholar 

  13. Wu T, Kayser B (2006) High altitude adaptation in Tibetans. High Alt Med Biol 7:193–208

    Article  PubMed  Google Scholar 

  14. Camps M, Castello A, Munoz P et al (1992) Effect of diabetes and fasting on GLUT-4 (muscle/fat) glucose-transporter expression in insulin-sensitive tissues. Heterogeneous response in heart, red and white muscle. Biochem J 282(Pt 3):765–772

    CAS  PubMed  Google Scholar 

  15. Severson DL (2004) Diabetic cardiomyopathy: recent evidence from mouse models of type 1 and type 2 diabetes. Can J Physiol Pharmacol 82:813–823

    Article  CAS  PubMed  Google Scholar 

  16. Bielawska AE, Shapiro JP, Jiang L et al (1997) Ceramide is involved in triggering of cardiomyocyte apoptosis induced by ischemia and reperfusion. Am J Pathol 151:1257–1263

    CAS  PubMed  Google Scholar 

  17. Chiu HC, Kovacs A, Blanton RM et al (2005) Transgenic expression of fatty acid transport protein 1 in the heart causes lipotoxic cardiomyopathy. Circ Res 96:225–233

    Article  CAS  PubMed  Google Scholar 

  18. Brandt JM, Djouadi F, Kelly DP (1998) Fatty acids activate transcription of the muscle carnitine palmitoyltransferase I gene in cardiac myocytes via the peroxisome proliferator-activated receptor alpha. J Biol Chem 273:23786–23792

    Article  CAS  PubMed  Google Scholar 

  19. Djouadi F, Brandt JM, Weinheimer CJ et al (1999) The role of the peroxisome proliferator-activated receptor alpha (PPAR alpha) in the control of cardiac lipid metabolism. Prostaglandins Leukot Essent Fatty Acids 60:339–343

    Article  CAS  PubMed  Google Scholar 

  20. Duncan JG, Bharadwaj KG, Fong JL et al (2010) Rescue of cardiomyopathy in peroxisome proliferator-activated receptor-alpha transgenic mice by deletion of lipoprotein lipase identifies sources of cardiac lipids and peroxisome proliferator-activated receptor-alpha activators. Circulation 121:426–435

    Article  CAS  PubMed Central  PubMed  Google Scholar 

  21. Narayanan S (1993) Aldose reductase and its inhibition in the control of diabetic complications. Ann Clin Lab Sci 23:148–158

    CAS  PubMed  Google Scholar 

  22. Wold LE, Ceylan-Isik AF, Ren J (2005) Oxidative stress and stress signaling: menace of diabetic cardiomyopathy. Acta Pharmacol Sin 26:908–917

    Article  CAS  PubMed  Google Scholar 

  23. Liu TP, Juang SW, Cheng JT et al (2005) The role of sorbitol pathway and treatment effect of aldose reductase inhibitor ONO2235 in the up-regulation of cardiac M2-muscarinic receptors in streptozotocin-induced diabetic rats. Neurosci Lett 383:131–135

    Article  CAS  PubMed  Google Scholar 

  24. Jiang T, Che Q, Lin Y et al (2006) Aldose reductase regulates TGF-beta1-induced production of fibronectin and type IV collagen in cultured rat mesangial cells. Nephrology (Carlton) 11: 105–112

    Article  CAS  Google Scholar 

  25. Young ME, Yan J, Razeghi P et al (2007) Proposed regulation of gene expression by glucose in rodent heart. Gene Regul Syst Bio 1:251–262

    PubMed  Google Scholar 

  26. Scognamiglio R, Avogaro A, Negut C et al (2004) Early myocardial dysfunction in the diabetic heart: current research and clinical applications. Am J Cardiol 93:17A–20A

    Article  CAS  PubMed  Google Scholar 

  27. Sack MN, Yellon DM (2003) Insulin therapy as an adjunct to reperfusion after acute coronary ischemia: a proposed direct myocardial cell survival effect independent of metabolic modulation. J Am Coll Cardiol 41:1404–1407

    Article  CAS  PubMed  Google Scholar 

  28. Jonassen AK, Mjos OD, Sack MN (2004) p70s6 kinase is a functional target of insulin activated Akt cell-survival signaling. Biochem Biophys Res Commun 315:160–165

    Article  CAS  PubMed  Google Scholar 

  29. Searls YM, Smirnova IV, Fegley BR et al (2004) Exercise attenuates diabetes-induced ultrastructural changes in rat cardiac tissue. Med Sci Sports Exerc 36:1863–1870

    Article  PubMed  Google Scholar 

  30. Weiss JN, Yang L, Qu Z (2006) Systems biology approaches to metabolic and cardiovascular disorders: network perspectives of cardiovascular metabolism. J Lipid Res 47:2355–2366

    Article  CAS  PubMed  Google Scholar 

  31. Swynghedauw B, Delcayre C, Samuel JL et al (2010) Molecular mechanisms in evolutionary cardiology failure. Ann N Y Acad Sci 1188:58–67

    Article  CAS  PubMed  Google Scholar 

  32. Durgan DJ, Young ME (2010) The cardiomyocyte circadian clock: emerging roles in health and disease. Circ Res 106:647–658

    Article  CAS  PubMed Central  PubMed  Google Scholar 

  33. Meng QJ, Logunova L, Maywood ES et al (2008) Setting clock speed in mammals: the CK1 epsilon tau mutation in mice accelerates circadian pacemakers by selectively destabilizing PERIOD proteins. Neuron 58:78–88

    Article  CAS  PubMed Central  PubMed  Google Scholar 

  34. Um JH, Yang S, Yamazaki S et al (2007) Activation of 5′-AMP-activated kinase with diabetes drug metformin induces casein kinase Iepsilon (CKIepsilon)-dependent degradation of clock protein mPer2. J Biol Chem 282:20794–20798

    Article  CAS  PubMed  Google Scholar 

  35. Bray MS, Young ME (2008) Diurnal variations in myocardial metabolism. Cardiovasc Res 79:228–237

    Article  CAS  PubMed  Google Scholar 

  36. Wallace DC, Fan W (2010) Energetics, epigenetics, mitochondrial genetics. Mitochondrion 10:12–31

    Article  CAS  PubMed Central  PubMed  Google Scholar 

  37. Villeneuve LM, Natarajan R (2010) The role of epigenetics in the pathology of diabetic complications. Am J Physiol Renal Physiol 299:F14–F25

    Article  CAS  PubMed  Google Scholar 

  38. Singh GB, Sharma R, Khullar M (2011) Epigenetics and diabetic cardiomyopathy. Diabetes Res Clin Pract 94:14–21

    Article  CAS  PubMed  Google Scholar 

  39. Asrih M, Steffens S (2012) Emerging role of epigenetics and miRNA in diabetic cardiomyopathy. Cardiovasc Pathol 22:117–125

    Article  PubMed  Google Scholar 

  40. Gaikwad AB, Sayyed SG, Lichtnekert J et al (2010) Renal failure increases cardiac histone h3 acetylation, dimethylation, and phosphorylation and the induction of cardiomyopathy-related genes in type 2 diabetes. Am J Pathol 176:1079–1083

    Article  CAS  PubMed  Google Scholar 

  41. El-Osta A, Brasacchio D, Yao D et al (2008) Transient high glucose causes persistent epigenetic changes and altered gene expression during subsequent normoglycemia. J Exp Med 205: 2409–2417

    Article  CAS  PubMed Central  PubMed  Google Scholar 

  42. Brasacchio D, Okabe J, Tikellis C et al (2009) Hyperglycemia induces a dynamic cooperativity of histone methylase and demethylase enzymes associated with gene-activating epigenetic marks that coexist on the lysine tail. Diabetes 58:1229–1236

    Article  CAS  PubMed  Google Scholar 

  43. Yu XY, Geng YJ, Lin QX et al (2010) High glucose leads to increased inflammatory gene expression via epigenetic histone H3 lysine 9 methylation in cardiomyocyte. Circulation 122: 8891–8898

    Article  Google Scholar 

  44. Movassagh M, Choy MK, Goddard M et al (2010) Differential DNA methylation correlates with differential expression of angiogenic factors in human heart failure. PLoS ONE 5:e8564

    Article  PubMed Central  PubMed  Google Scholar 

  45. Kao YH, Chen YC, Cheng CC et al (2010) Tumor necrosis factor-alpha decreases sarcoplasmic reticulum Ca2+-ATPase expressions via the promoter methylation in cardiomyocytes. Crit Care Med 38:217–222

    Article  CAS  PubMed  Google Scholar 

  46. Kuan CJ, al-Douahji M, Shankland SJ (1998) The cyclin kinase inhibitor p21WAF1, CIP1 is increased in experimental diabetic nephropathy: potential role in glomerular hypertrophy. J Am Soc Nephrol 9:986–993

    CAS  PubMed  Google Scholar 

  47. Kaneto H, Kajimoto Y, Fujitani Y et al (1999) Oxidative stress induces p21 expression in pancreatic islet cells: possible implication in beta-cell dysfunction. Diabetologia 42:1093–1097

    Article  CAS  PubMed  Google Scholar 

  48. Yu XY, Geng YJ, Liang JL et al (2010) High levels of glucose induce apoptosis in cardiomyocyte via epigenetic regulation of the insulin-like growth factor receptor. Exp Cell Res 316: 2903–2909

    Article  CAS  PubMed  Google Scholar 

  49. Cheng Y, Liu G, Pan Q et al (2011) Elevated expression of liver X receptor alpha in myocardium of streptozotocin induced diabetic rats. Inflammation 34:698–706

    Article  CAS  PubMed  Google Scholar 

  50. Hausenloy DJ, Yellon DM (2004) New directions for protecting the heart against ischaemia-reperfusion injury: targeting the Reperfusion Injury Salvage Kinase (RISK)-pathway. Cardiovasc Res 61:448–460

    Article  CAS  PubMed  Google Scholar 

  51. Fuglesteg BN, Suleman N, Tiron C et al (2008) Signal transducer and activator of transcription 3 is involved in the cardioprotective signalling pathway activated by insulin therapy at reperfusion. Basic Res Cardiol 103:444–453

    Article  CAS  PubMed Central  PubMed  Google Scholar 

  52. Vahtola E, Louhelainen M, Forsten H et al (2010) Sirtuin1-p53, forkhead box O3a, p38 and post-infarct cardiac remodeling in the spontaneously diabetic Goto-Kakizaki rat. Cardiovasc Diabetol 9:5

    Article  PubMed Central  PubMed  Google Scholar 

  53. Berezikov E (2011) Evolution of microRNA diversity and regulation in animals. Nat Rev Genet 12:846–860

    Article  CAS  PubMed  Google Scholar 

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Author information

Authors and Affiliations

  1. Department of Pathology, Aberdeen Royal Infirmary, Foresterhill, Aberdeen, Scotland

    Vijay Sharma

  2. Division of Applied Medicine, School of Medicine and Dentistry, The University of Aberdeen, Aberdeen, Scotland

    Vijay Sharma

  3. BMJ Evidence Centre, BMJ Group, BMA House, Tavistock Square, London, UK

    Vijay Sharma

  4. Faculty of Pharmaceutical Sciences, University of British Columbia, Vancouver, BC, V6T 1Z3, Canada

    John H. McNeill

Authors
  1. Vijay Sharma
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  2. John H. McNeill
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Corresponding author

Correspondence to John H. McNeill .

Editor information

Editors and Affiliations

  1. Department of Biophysics, University of Ankara, Ankara, Ankara, Turkey

    Belma Turan

  2. St. Boniface Hosp. Research, Univ. of Ma Institute of Cardiovascular Sciences, Winnipeg, Manitoba, Canada

    Naranjan S. Dhalla

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Sharma, V., McNeill, J.H. (2014). Metabolic and Contractile Remodelling in the Diabetic Heart: An Evolutionary Perspective. In: Turan, B., Dhalla, N. (eds) Diabetic Cardiomyopathy. Advances in Biochemistry in Health and Disease, vol 9. Springer, New York, NY. https://doi.org/10.1007/978-1-4614-9317-4_2

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