Free Access
Issue
Med Sci (Paris)
Volume 34, Number 6-7, Juin–Juillet 2018
Les Cahiers de Myologie
Page(s) 563 - 570
Section M/S Revues
DOI https://doi.org/10.1051/medsci/20183406016
Published online 31 July 2018
  1. Fosse-Edorh S, Mandereau-Bruno L, Regnault N. Le poids des complications liées au diabète en France en 2013. Synthèse et perspectives. Bull Epidemiol Hebd 2015 ; 34–35 : 619–625. [Google Scholar]
  2. Haute Autorité de Santé. Prévention et dépistage du diabète de type 2 et des maladies liées au diabète. Paris : HAS, 2014. [Google Scholar]
  3. Organisation Mondiale de la Santé. Rapport mondial sur le diabète. Genève : OMS, 2016. [Google Scholar]
  4. Danaei G, Finucane MM, Lu Y, Singh GM. et al. National, regional, and global trends in fasting plasma glucose and diabetes prevalence since 1980: systematic analysis of health examination surveys and epidemiological studies with 370 country-years and 2·7 million participants. Lancet Lond Engl 2011 ; 378 : 31–40. [Google Scholar]
  5. Aneja A, Tang WHW, Bansilal S. et al. Diabetic cardiomyopathy: insights into pathogenesis, diagnostic challenges, and therapeutic options. Am J Med 2008 ; 121 : 748–757. [Google Scholar]
  6. MacDonald MR, Jhund PS, Petrie MC. et al. Discordant short- and long-term outcomes associated with diabetes in patients with heart failure: importance of age and sex. Clinical Perspective: A population study of 5.1 million people in Scotland. Circ Heart Fail 2008 ; 1 : 234–241. [CrossRef] [PubMed] [Google Scholar]
  7. Stanley WC, Recchia FA, Lopaschuk GD. Myocardial substrate metabolism in the normal and failing heart. Physiol Rev 2005 ; 85 : 1093–1129. [Google Scholar]
  8. Bertrand L, Horman S, Beauloye C. et al. Insulin signalling in the heart. Cardiovasc Res 2008 ; 79 : 238–248. [CrossRef] [PubMed] [Google Scholar]
  9. Young ME, McNulty P, Taegtmeyer H. Adaptation and maladaptation of the heart in diabetes. Part II: potential mechanisms. Circulation 2002 ; 105 : 1861–1870. [CrossRef] [PubMed] [Google Scholar]
  10. Abel ED, O’Shea KM, Ramasamy R. Insulin resistance: metabolic mechanisms and consequences in the heart. Arterioscler Thromb Vasc Biol 2012 ; 32 : 2068–2076. [CrossRef] [PubMed] [Google Scholar]
  11. Zlobine I, Gopal K, Ussher JR. Lipotoxicity in obesity and diabetes-related cardiac dysfunction. Biochim Biophys Acta 2016 ; 1861 : 1555–1568. [CrossRef] [PubMed] [Google Scholar]
  12. Kolwicz SC, Tian R. Glucose metabolism and cardiac hypertrophy. Cardiovasc Res 2011 ; 90 : 194–201. [CrossRef] [PubMed] [Google Scholar]
  13. Elder DHJ, Singh JSS, Levin D. et al. Mean HbA1c and mortality in diabetic individuals with heart failure: a population cohort study. Eur J Heart Fail 2016 ; 18 : 94–102. [CrossRef] [PubMed] [Google Scholar]
  14. Montaigne D, Marechal X, Coisne A. et al. Myocardial contractile dysfunction is associated with impaired mitochondrial function and dynamics in type 2 diabetic but not in obese patients. Circulation 2014 ; 130 : 554–564. [CrossRef] [PubMed] [Google Scholar]
  15. Dyntar D, Sergeev P, Klisic J. et al. High glucose alters cardiomyocyte contacts and inhibits myofibrillar formation. J Clin Endocrinol Metab 2006 ; 91 : 1961–1967. [CrossRef] [PubMed] [Google Scholar]
  16. Sen S, Kundu BK, Wu HC. et al. Glucose regulation of load-induced mTOR signaling and ER stress in mammalian heart. J Am Heart Assoc Cardiovasc Cerebrovasc Dis 2013 ; 2 : e004796. [Google Scholar]
  17. Cai L, Li W, Wang G. et al. Hyperglycemia-induced apoptosis in mouse Mmyocardium: mitochondrial cytochrome c-mediated caspase-3 activation pathway. Diabetes 2002 ; 51 : 1938–1948. [CrossRef] [PubMed] [Google Scholar]
  18. Tian C, Alomar F, Moore CJ. et al. Reactive carbonul species and their roles in sarcoplasmic reticulum Ca2+ cycling defect in the diabetic heart. Heart Fail Rev 2014 ; 19 : 101–112. [CrossRef] [PubMed] [Google Scholar]
  19. Shao CH, Rozanski GJ, Patel KP. et al. Dyssynchronous (non-uniform) Ca2+ release in myocytes from streptozotocin-induced diabetic rats. J Mol Cell Cardiol 2007 ; 42 : 234–246. [CrossRef] [PubMed] [Google Scholar]
  20. Thornalley PJ, Langborg A, Minhas HS. Formation of glyoxal, methylglyoxal and 3-deoxyglucosone in the glycation of proteins by glucose. Biochem J 1999 ; 344 : 109–116. [CrossRef] [PubMed] [Google Scholar]
  21. Brahma MK, Pepin ME, Wende AR. My Sweetheart is broken: role of glucose in diabetic cardiomyopathy. Diabetes Metab J 2017 ; 41 : 1–9. [CrossRef] [PubMed] [Google Scholar]
  22. Wright JN, Collins HE, Wende AR. et al. O-GlcNAcylation and cardiovascular disease. Biochem Soc Trans 2017 ; 45 : 545–553. [CrossRef] [PubMed] [Google Scholar]
  23. Ramirez-Correa GA, Jin W, Wang Z. et al. O-linked GlcNAc modification of cardiac myofilament proteins: A novel regulator of myocardial contractile function. Circ Res 2008 ; 103 : 1354–1358. [PubMed] [Google Scholar]
  24. Hu Y, Suarez J, Fricovsky E. et al. Increased enzymatic O-GlcNAcylation of mitochondrial proteins impairs mitochondrial function in cardiac myocytes exposed to high glucose. J Biol Chem 2009 ; 284 : 547–555. [CrossRef] [PubMed] [Google Scholar]
  25. Joubert M, Jagu B, Montaigne D. et al. The sodium–glucose cotransporter 2 inhibitor dapagliflozin prevents cardiomyopathy in a diabetic lipodystrophic mouse model. Diabetes 2017 ; 66 : 1030–1040. [CrossRef] [PubMed] [Google Scholar]
  26. Magré J, Delépine M, Khallouf E. et al. Identification of the gene altered in Berardinelli-Seip congenital lipodystrophy on chromosome 11q13. Nat Genet 2001 ; 28 : 365–370. [Google Scholar]
  27. Szymanski KM, Binns D, Bartz R. et al. The lipodystrophy protein seipin is found at endoplasmic reticulum lipid droplet junctions and is important for droplet morphology. Proc Natl Acad Sci USA 2007 ; 104 : 20890–20895. [CrossRef] [Google Scholar]
  28. Cartwright BR, Goodman JM. Seipin: from human disease to molecular mechanism. J Lipid Res 2012 ; 53 : 1042–1055. [CrossRef] [PubMed] [Google Scholar]
  29. Agarwal AK, Arioglu E, De Almeida S. et al. AGPAT2 is mutated in congenital generalized lipodystrophy linked to chromosome 9q34. Nat Genet 2002 ; 31 : 21–23. [Google Scholar]
  30. Lupsa BC, Sachdev V, Lungu AO. et al. Cardiomyopathy in congenital and acquired generalized lipodystrophy. Medicine (Baltimore) 2010 ; 89 : 245–250. [CrossRef] [PubMed] [Google Scholar]
  31. Agarwal AK, Simha V, Oral EA. et al. Phenotypic and genetic heterogeneity in congenital generalized lipodystrophy. J Clin Endocrinol Metab 2003 ; 88 : 4840–4847. [CrossRef] [PubMed] [Google Scholar]
  32. Cui X, Wang Y, Tang Y. et al. Seipin ablation in mice results in severe generalized lipodystrophy. Hum Mol Genet 2011 ; 20 : 3022–3030. [CrossRef] [PubMed] [Google Scholar]
  33. Chen W, Chang B, Saha P. et al. Berardinelli-Seip congenital lipodystrophy 2/seipin is a cell-autonomous regulator of lipolysis essential for adipocyte differentiation. Mol Cell Biol 2012 ; 32 : 1099–1111. [CrossRef] [PubMed] [Google Scholar]
  34. Prieur X, Dollet L, Takahashi M. et al. Thiazolidinediones partially reverse the metabolic disturbances observed in Bscl2/seipin-deficient mice. Diabetologia 2013 ; 56 : 1813–1825. [CrossRef] [PubMed] [Google Scholar]
  35. Chistiakov DA, Orekhov AN, Bobryshev YV. The impact of FOXO-1 to cardiac pathology in diabetes mellitus and diabetes-related metabolic abnormalities. Int J Cardiol 2017 ; 245 : 236–244. [CrossRef] [PubMed] [Google Scholar]
  36. Ferrannini E. Sodium-glucose co-transporters and their inhibition: clinical physiology. Cell Metab 2017 ; 26 : 27–38. [CrossRef] [PubMed] [Google Scholar]
  37. Zinman B, Wanner C, Lachin JM. et al. Empagliflozin, cardiovascular outcomes, and mortality in type 2 diabetes. EMPA-REG outcome investigators. N Engl J Med 2015 ; 373 : 2117–2128. [Google Scholar]
  38. Neal B, Perkovic V, Mahaffey KW. et al. Canagliflozin and cardiovascular and renal events in type 2 diabetes. N Engl J Med 2017 ; 377 : 644–657. [Google Scholar]
  39. Staels B. Cardiovascular protection by sodium glucose cotransporter 2 inhibitors: potential mechanisms. Am J Cardiol 2017 ; 120 : S28–S36. [CrossRef] [PubMed] [Google Scholar]
  40. Taylor SI, Blau JE, Rother KI. SGLT2 Inhibitors may predispose to ketoacidosis. J Clin Endocrinol Metab 2015 ; 100 : 2849–2852. [CrossRef] [PubMed] [Google Scholar]
  41. Ferrannini E, Mark M, Mayoux E. CV Protection in the EMPA-REG OUTCOME trial: a Thrifty substrate hypothesis. Diabetes Care 2016 ; 39 : 1108–1114. [CrossRef] [PubMed] [Google Scholar]
  42. Liljenquist JE, Bomboy JD, Lewis SB. et al. Effects of glucagon on lipolysis and ketogenesis in normal and diabetic men. J Clin Invest 1974 ; 53 : 190–197. [CrossRef] [PubMed] [Google Scholar]
  43. Sato K, Kashiwaya Y, Keon CA. et al. Insulin, ketone bodies, and mitochondrial energy transduction. FASEB J 1995 ; 9 : 651–658. [CrossRef] [PubMed] [Google Scholar]
  44. Scheen AJ, Delanaye P. Effects of reducing blood pressure on renal outcomes in patients with type 2 diabetes: focus on SGLT2 inhibitors and EMPA-REG OUTCOME. Diabetes Metab 2017 ; 43 : 99–109. [CrossRef] [PubMed] [Google Scholar]
  45. Nicolas S, Chabry J, Guyon A. et al. L’adiponectine : un anti-inflammatoire et antidépresseur endogène ?. Med Sci (Paris) 2018 ; 34 : 417–423. [CrossRef] [EDP Sciences] [PubMed] [Google Scholar]
  46. Marcelin G, Clément K. La fibrose du tissu adipeux : un facteur aggravant de l’obésité. Med Sci (Paris) 2018 ; 34 : 424–431. [CrossRef] [EDP Sciences] [PubMed] [Google Scholar]

Current usage metrics show cumulative count of Article Views (full-text article views including HTML views, PDF and ePub downloads, according to the available data) and Abstracts Views on Vision4Press platform.

Data correspond to usage on the plateform after 2015. The current usage metrics is available 48-96 hours after online publication and is updated daily on week days.

Initial download of the metrics may take a while.