Consequences of exercising on ischemia-reperfusion injury in type 2 diabetic Goto-Kakizaki rat hearts role of the HO/NOS system /
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 exercis...
Elmentve itt :
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| Dokumentumtípus: | Cikk |
| Megjelent: |
2015
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| Sorozat: | DIABETOLOGY AND METABOLIC SYNDROME
7 No. 1 |
| doi: | 10.1186/s13098-015-0080-x |
| mtmt: | 2963305 |
| Online Access: | http://publicatio.bibl.u-szeged.hu/7599 |
| Tartalmi kivonat: | 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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| Terjedelem/Fizikai jellemzők: | Terjedelem: 9 p.-Azonosító: 85 |
| ISSN: | 1758-5996 |