Consequences of exercising on ischemia-reperfusion injury in type 2 diabetic Goto-Kakizaki rat hearts

Role of the HO/NOS system

Krisztina Kupai, Renáta Szabó, Médea Veszelka, Amin Al Awar, Szilvia Török, Anett Csonka, Zoltán Baráth, A. Pósa, C. Varga

Research output: Contribution to journalArticle

6 Citations (Scopus)

Abstract

Background: It is well established that physical exercise continues to be one of the most valuable forms of non-pharmacological therapy against diabetes mellitus; however, the precise mechanism remains unknown. The aim of this study was to investigate the cardioprotective effect of voluntary exercise in the Goto-Kakizaki type 2 diabetic rat heart against ischemia-reperfusion injury and to clarify its biochemical background, focusing on the nitric oxide synthase/heme oxygenase system. Methods: One group of male Goto-Kakizaki rats were allowed voluntary exercise, whereas others were kept sedentary for 6 weeks. At the end of the 6th week the hearts were isolated from both groups and subjected to 45-min coronary occlusion followed by 120-min reperfusion. The infarct size was evaluated by means of triphenyltetrazolium chloride staining. The cardiac and aortic nitric oxide synthase/heme oxygenase activities, plasma leptin and glucose concentrations were also assessed. Results: The sedentary state prior to the ischemia-reperfusion injury was associated with a significantly higher infarct size (24.56 ± 2.21 vs. 16.66 ± 1.87 %) as compared with that in the voluntary wheel-running group. Exercise altered the constitutive nitric oxide synthase activity; an enhancement was evident in the cardiac (42.5 ± 2.72 vs. 75.6 ± 13.34 pmol/min/mg protein) and aortic tissues (382.5 ± 66.57 vs. 576.9 ± 63.16 pmol/min/mg protein). Exercise lead to a higher heme oxygenase activity (0.68 ± 0.08 vs. 0.92 ± 0.04 nmol bilirubin/h/mg protein) in the diabetic rat hearts. Exercise was associated with lower plasma leptin (192.23 ± 7.22 vs. 169.65 ± 4.6 ng/L) and blood glucose (19.61 ± 0.76 vs. 14.58 ± 0.88 mmol/L) levels. Conclusions: These results indicate the beneficial role of exercise against myocardial ischemia-reperfusion injury in diabetic rats. These observations in experimental diabetes suggest that the cytoprotective mechanism of exercise involves modulation of the nitric oxide synthase/heme oxygenase system and metabolic parameters that may be responsible for cardioprotection.

Original languageEnglish
Article number85
JournalDiabetology and Metabolic Syndrome
Volume7
Issue number1
DOIs
Publication statusPublished - Oct 6 2015

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Heme Oxygenase (Decyclizing)
Reperfusion Injury
Nitric Oxide Synthase
Leptin
Myocardial Reperfusion Injury
Glucose
Proteins
Coronary Occlusion
Bilirubin
Running
Reperfusion
Myocardial Ischemia
Blood Glucose
Diabetes Mellitus
Exercise
Staining and Labeling
Therapeutics

Keywords

  • Exercise
  • Heme oxygenase
  • Ischemia-reperfusion
  • Nitric oxide synthase

ASJC Scopus subject areas

  • Endocrinology, Diabetes and Metabolism
  • Internal Medicine

Cite this

Consequences of exercising on ischemia-reperfusion injury in type 2 diabetic Goto-Kakizaki rat hearts : Role of the HO/NOS system. / Kupai, Krisztina; Szabó, Renáta; Veszelka, Médea; Awar, Amin Al; Török, Szilvia; Csonka, Anett; Baráth, Zoltán; Pósa, A.; Varga, C.

In: Diabetology and Metabolic Syndrome, Vol. 7, No. 1, 85, 06.10.2015.

Research output: Contribution to journalArticle

Kupai, Krisztina ; Szabó, Renáta ; Veszelka, Médea ; Awar, Amin Al ; Török, Szilvia ; Csonka, Anett ; Baráth, Zoltán ; Pósa, A. ; Varga, C. / Consequences of exercising on ischemia-reperfusion injury in type 2 diabetic Goto-Kakizaki rat hearts : Role of the HO/NOS system. In: Diabetology and Metabolic Syndrome. 2015 ; Vol. 7, No. 1.
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N2 - Background: It is well established that physical exercise continues to be one of the most valuable forms of non-pharmacological therapy against diabetes mellitus; however, the precise mechanism remains unknown. The aim of this study was to investigate the cardioprotective effect of voluntary exercise in the Goto-Kakizaki type 2 diabetic rat heart against ischemia-reperfusion injury and to clarify its biochemical background, focusing on the nitric oxide synthase/heme oxygenase system. Methods: One group of male Goto-Kakizaki rats were allowed voluntary exercise, whereas others were kept sedentary for 6 weeks. At the end of the 6th week the hearts were isolated from both groups and subjected to 45-min coronary occlusion followed by 120-min reperfusion. The infarct size was evaluated by means of triphenyltetrazolium chloride staining. The cardiac and aortic nitric oxide synthase/heme oxygenase activities, plasma leptin and glucose concentrations were also assessed. Results: The sedentary state prior to the ischemia-reperfusion injury was associated with a significantly higher infarct size (24.56 ± 2.21 vs. 16.66 ± 1.87 %) as compared with that in the voluntary wheel-running group. Exercise altered the constitutive nitric oxide synthase activity; an enhancement was evident in the cardiac (42.5 ± 2.72 vs. 75.6 ± 13.34 pmol/min/mg protein) and aortic tissues (382.5 ± 66.57 vs. 576.9 ± 63.16 pmol/min/mg protein). Exercise lead to a higher heme oxygenase activity (0.68 ± 0.08 vs. 0.92 ± 0.04 nmol bilirubin/h/mg protein) in the diabetic rat hearts. Exercise was associated with lower plasma leptin (192.23 ± 7.22 vs. 169.65 ± 4.6 ng/L) and blood glucose (19.61 ± 0.76 vs. 14.58 ± 0.88 mmol/L) levels. Conclusions: These results indicate the beneficial role of exercise against myocardial ischemia-reperfusion injury in diabetic rats. These observations in experimental diabetes suggest that the cytoprotective mechanism of exercise involves modulation of the nitric oxide synthase/heme oxygenase system and metabolic parameters that may be responsible for cardioprotection.

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