The effect of high-fructose feeding on hemodynamic behavior and infarct size of isolated rat hearts subjected to low-flow ischemia.

Year 2022, , 324 - 329, 01.08.2022

Serap Topçu Özen Orkide Palabıyık , Zuhal Guksu , Enver Arslan , Esra Akbaş Tosunoğlu Necdet Süt , Selma Arzu Vardar

https://doi.org/10.54005/geneltip.1095947

Cited By: 1

Abstract

Objective: The aim of this study was to investigate the potentially deleterious effect of in vivo high-fructose feeding of rats on ex vivo hemodynamic recovery and infarct size of isolated rat hearts subjected to low-flow ischemia and reperfusion.
Methods: After feeding Sprague-Dawley male rats with a high-fructose (n=9), high-glucose (n=9) or a standard diet (n=9) for four weeks, the hearts were extirpated and perfused ex vivo with a Krebs-Henseleit solution for 15 min; thereafter the hearts were subjected to low flow (0.3 ml/min) ischemia during 30 min followed by 60 min reperfusion. Left ventricular developed pressure (LVDP), first derivative of pressure development during the contraction and relaxation phase and heart rate were recorded prior to ischemia and after reperfusion. Infarct area was measured at the end of the reperfusion period.
Results: In isolated hearts, subjected to ex vivo low-flow ischemia followed by 60 min reperfusion, the relative myocardial infarct size did not differ between the three groups. Post-ischemic cardiac contractile recovery appeared to be complete in both the high-fructose and high-glucose group at 60 min reperfusion. In contrast, in the control group LVDP and left ventricular relaxation rate were still depressed at the end of 60 minutes of reperfusion.
Conclusion: Feeding with a high-fructose diet of rats appears to have a positive effect on the recovery of left ventricular contractile function after low-flow ischemia, in comparison to a standard diet, without a difference in relative myocardial infarct size. Similar results were obtained in the high-glucose fed rats.

Keywords

frucrose, rat, heart, myocardial ischemia, reperfusion, hemodynamic function, infact size

Supporting Institution

This study is supported by the foundation of Trakya (Scientific Research Projects Office of Trakya University).

Project Number

Project number:2012/27

Düşük Akımlı İskemiye Maruz Kalan İzole Sıçan Kalplerinde Yüksek Fruktoz ile Beslenmenin Hemodinamik Davranış ve Enfarktüs Boyutu Üzerine Etkisi

Abstract

Amaç: Bu çalışmanın amacı, düşük akımlı iskemi ve reperfüzyona maruz bırakılan izole sıçan kalplerinde in vivo yüksek fruktozla beslenmenin, ex vivo hemodinamik iyileşme ve enfarktüs boyutu üzerindeki potansiyel zararlı etkisini araştırmaktı.
Gereç ve Yöntemler: Erkek Sprague-Dawley sıçanları dört hafta boyunca yüksek fruktozlu (n=9), yüksek glikozlu (n=9) veya standart bir diyetle (n=9) besledikten sonra, kalpleri çıkarıldı ve Krebs-Henseleit solüsyonu ile 15 dakika ex vivo perfüze edildi. Daha sonra kalpler, 30 dakika boyunca düşük akımlı (0.3 ml/dk) iskemiye ve ardından 60 dakikalık reperfüzyona tabi tutuldu. Sol ventrikül gelişim basıncı (SVGB), kasılma ve gevşeme fazındaki basınç gelişim oranları ve kalp hızı iskemi öncesi ve reperfüzyon sonrası kaydedildi. Enfarktüs alanı reperfüzyon periyodunun sonunda ölçüldü.
Bulgular: Ex vivo düşük akımlı iskemiye tabi tutulan izole kalplerde 60 dakikalık reperfüzyonun ardından, miyokard enfarktüsü boyutu üç grup arasında farklılık göstermedi. İskemi sonrası kardiyak kontraktil iyileşmenin hem yüksek fruktoz hem de yüksek glikoz grubunda 60 dakikalık reperfüzyonda tamamlanmış olduğu görüldü. Buna karşılık, kontrol grubunda LVDP ve sol ventrikül gevşeme hızı, 60 dakikalık reperfüzyonun sonunda hala baskılanmış durumdaydı.
Sonuç: Sıçanları yüksek fruktozlu diyetiyle beslenmenin, standart bir diyete kıyasla, miyokard enfarktüsü boyutunda bir fark olmaksızın, düşük akımlı iskemiden sonra sol ventrikül kontraktil fonksiyonunun iyileşmesi üzerinde olumlu bir etkisi olduğu görülmektedir. Yüksek glikozla beslenen sıçanlarda da benzer sonuçlar elde edildi.

Keywords

fruktoz, sıçan, kalp, miyokardiyal iskemi, reperfüzyon, hemodinamik fonksiyon, entarktüs boyutu

Project Number

Project number:2012/27

References

• 1. Miller A, Adeli K. Dietary fructose and the metabolic syndrome. Curr Opin Gastroenterol. 2008;24(2):204-9.
• 2. Basciano H, Federico L, Adeli K. Fructose, insulin resistance, and metabolic dyslipidemia. Nutr Metab (Lond). 2005;2(1):1-14.
• 3. Malik VS, Hu FB. Fructose and cardiometabolic health: what the evidence from sugar-sweetened beverages tells us. J Am Coll Cardiol. 2015;66(14):1615-24.
• 4. Bray GA, Popkin BM. Dietary sugar and body weight: have we reached a crisis in the epidemic of obesity and diabetes?: health be damned! Pour on the sugar. Diabetes care. 2014;37(4):950-6.
• 5. Stanhope KL. Role of fructose-containing sugars in the epidemics of obesity and metabolic syndrome. Annu Rev Med. 2012;63:329-43.
• 6. Toop CR, Gentili S. Fructose beverage consumption induces a metabolic syndrome phenotype in the rat: a systematic review and meta-analysis. Nutrients. 2016;8(9):577.
• 7. Bahadoran Z, Mirmiran P, Tohidi M, Azizi F. Longitudinal associations of high-fructose diet with cardiovascular events and potential risk factors: Tehran Lipid and Glucose Study. Nutrients. 2017;9(8):872.
• 8. Mellor KM, Bell JR, Wendt IR, et al. Fructose modulates cardiomyocyte excitation-contraction coupling and Ca 2+ handling in vitro. PLoS One. 2011;6(9):e25204.
• 9. Bundalo M, Romic S, Tepavcevic S, et al. Fructose-rich diet and insulin action in female rat heart: Estradiol friend or foe? Eur J Pharmacol. 2017;811:141-7.
• 10. Delbridge LM, Benson VL, Ritchie RH, Mellor KM. Diabetic cardiomyopathy: the case for a role of fructose in disease etiology. Diabetes. 2016;65(12):3521-8.
• 11. Miller AW, Katakam PV, Ujhelyi MR. Impaired Endothelium-Mediated Relaxation in Coronary Arteries from Insulin-Resistant Rats1. J Vasc Res. 1999;36(5):385-92.
• 12. Jordan JE, Simandle SA, Tulbert CD, Busija DW, Miller AW. Fructose-fed rats are protected against ischemia/reperfusion injury. J Pharmacol Exp Ther. 2003;307(3):1007-11.
• 13. Faure MJ, Rossini E, Ribuot C, Faure P. Fructose-fed rat hearts are protected against ischemia-reperfusion injury. Exp Biol Med. 2006;231(4):456-62.
• 14. Azari MH, Najafi M. Role of fructose as a potent antiarrhythmic and anti-infarct agent in isolated rat heart. Iran J Pharm Res. 2014;13(4):1303.
• 15. Haghi J, Eteraf-Oskouei T, Najafi M. Effects of postconditioning with fructose on arrhythmias and the size of infarct caused by global ischemia and reperfusion in isolated rat heart. Adv Pharm Bull. 2018;8(1):57.
• 16. Karaca A, Palabıyık O, Taştekin E, Turan FN, Vardar SA. High fructose diet suppresses exercise-induced increase in AQP7 expression in the in vivo rat heart. Anatol J Cardiol. 2016;16(12):916.
• 17. Hausenloy DJ, Duchen MR, Yellon DM. Inhibiting mitochondrial permeability transition pore opening at reperfusion protects against ischaemia–reperfusion injury. Cardiovasc res. 2003;60(3):617-25.
• 18. Lloyd SG, Wang P, Zeng H, Chatham JC. Impact of low-flow ischemia on substrate oxidation and glycolysis in the isolated perfused rat heart. Am J Physiol Heart Circ Physiol. 2004;287(1):H351-H62.
• 19. Skrzypiec-Spring M, Grotthus B, Szeląg A, Schulz R. Isolated heart perfusion according to Langendorff—still viable in the new millennium. J Pharmacol Toxicol Methods. 2007;55(2):113-26.
• 20. Downey J. Measuring infarct size by the tetrazolium method. The ISHR Handbook of Experimental Laboratory Procedures Downey JM, ed International Society of Heart Disease. 2000.
• 21. Sakr H. Modulation of metabolic and cardiac dysfunctions by swimming in overweight rats on a high cholesterol and fructose diet: Possible role of adiponectin. J Physiol Pharmacol. 2013;64(2):231-40.
• 22. Mellor KM, Wendt IR, Ritchie RH, Delbridge LM. Fructose diet treatment in mice induces fundamental disturbance of cardiomyocyte Ca2+ handling and myofilament responsiveness. Am J Physiol Heart Circ Physiol. 2012;302(4):H964-H72.
• 23. Xing S-S, Bi X-P, Tan H-W, et al. Overexpression of interleukin-18 aggravates cardiac fibrosis and diastolic dysfunction in fructose-fed rats. Mol Med. 2010;16(11):465-70.
• 24. Morel S, Berthonneche C, Tanguy S, et al. Insulin resistance modifies plasma fatty acid distribution and decreases cardiac tolerance to in vivo ischaemia/reperfusion in rats. Clin Exp Pharmacol Physiol. 2003;30(7):446-51.
• 25. Chess DJ, Lei B, Hoit BD, Azimzadeh AM, Stanley WC. Deleterious effects of sugar and protective effects of starch on cardiac remodeling, contractile dysfunction, and mortality in response to pressure overload. Am J Physiol Heart Circ Physiol. 2007.
• 26. Softic S, Gupta MK, Wang G-X, et al. Divergent effects of glucose and fructose on hepatic lipogenesis and insulin signaling. J Clin Invest. 2017;127(11):4059-74.
• 27. Schaefer EJ, Gleason JA, Dansinger ML. Dietary fructose and glucose differentially affect lipid and glucose homeostasis. J Nutr. 2009;139(6):1257S-62S.
• 28. Stanhope KL, Havel PJ. Fructose consumption: potential mechanisms for its effects to increase visceral adiposity and induce dyslipidemia and insulin resistance. Curr Opin Lipidol. 2008;19(1):16.
• 29. Leˆ K-A, Faeh D, Stettler R, et al. A 4-wk high-fructose diet alters lipid metabolism without affecting insulin sensitivity or ectopic lipids in healthy humans. Am J Clin Nutr. 2006;84(6):1374-9.
• 30. Silbernagel G, Lütjohann D, Machann J, et al. Cholesterol synthesis is associated with hepatic lipid content and dependent on fructose/glucose intake in healthy humans. Exp Diabetes Res. 2011;2012.
• 31. Yang Q, Zhang Z, Gregg EW, et al. Added sugar intake and cardiovascular diseases mortality among US adults. JAMA Intern Med. 2014;174(4):516-24.