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Consequences of exercising on ischemia-reperfusion injury in type 2 diabetic Goto-Kakizaki rat hearts: role of the HO/NOS system.

Kupai K, Szabó R, Veszelka M, Awar AA, Török S, Csonka A, Baráth Z, Pósa A, Varga C - Diabetol Metab Syndr (2015)

Bottom Line: 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.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.

View Article: PubMed Central - PubMed

Affiliation: Department of Physiology, Anatomy and Neuroscience, Faculty of Science and Informatics, University of Szeged, Kozep fasor 52, 6726 Szeged, Hungary.

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.

No MeSH data available.


Related in: MedlinePlus

The constitutive nitric oxide synthase (cNOS) activities (expressed in pmol/min/mg protein) in the a heart and b aorta of GK rats at the end of the 6-week exercise or sedentary period. Data are mean ± SEM. Statistical significance: *p < 0.05 relative to the GK sed group. GK sed sedentary Goto-Kakizaki rats, GK run voluntary wheel-running Goto-Kakizaki rats
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Fig5: The constitutive nitric oxide synthase (cNOS) activities (expressed in pmol/min/mg protein) in the a heart and b aorta of GK rats at the end of the 6-week exercise or sedentary period. Data are mean ± SEM. Statistical significance: *p < 0.05 relative to the GK sed group. GK sed sedentary Goto-Kakizaki rats, GK run voluntary wheel-running Goto-Kakizaki rats

Mentions: After the 6 weeks of exercise, the cNOS activity was significantly higher both in the heart (42.5 ± 2.72 vs. 75.6 ± 13.34 pmol/min/mg protein) and in the aorta (382.5 ± 66.57 vs. 576.9 ± 63.16 pmol/min/mg protein) relative to the sedentary control group (Fig. 5).Fig. 5


Consequences of exercising on ischemia-reperfusion injury in type 2 diabetic Goto-Kakizaki rat hearts: role of the HO/NOS system.

Kupai K, Szabó R, Veszelka M, Awar AA, Török S, Csonka A, Baráth Z, Pósa A, Varga C - Diabetol Metab Syndr (2015)

The constitutive nitric oxide synthase (cNOS) activities (expressed in pmol/min/mg protein) in the a heart and b aorta of GK rats at the end of the 6-week exercise or sedentary period. Data are mean ± SEM. Statistical significance: *p < 0.05 relative to the GK sed group. GK sed sedentary Goto-Kakizaki rats, GK run voluntary wheel-running Goto-Kakizaki rats
© Copyright Policy - OpenAccess
Related In: Results  -  Collection

License 1 - License 2
Show All Figures
getmorefigures.php?uid=PMC4595319&req=5

Fig5: The constitutive nitric oxide synthase (cNOS) activities (expressed in pmol/min/mg protein) in the a heart and b aorta of GK rats at the end of the 6-week exercise or sedentary period. Data are mean ± SEM. Statistical significance: *p < 0.05 relative to the GK sed group. GK sed sedentary Goto-Kakizaki rats, GK run voluntary wheel-running Goto-Kakizaki rats
Mentions: After the 6 weeks of exercise, the cNOS activity was significantly higher both in the heart (42.5 ± 2.72 vs. 75.6 ± 13.34 pmol/min/mg protein) and in the aorta (382.5 ± 66.57 vs. 576.9 ± 63.16 pmol/min/mg protein) relative to the sedentary control group (Fig. 5).Fig. 5

Bottom Line: 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.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.

View Article: PubMed Central - PubMed

Affiliation: Department of Physiology, Anatomy and Neuroscience, Faculty of Science and Informatics, University of Szeged, Kozep fasor 52, 6726 Szeged, Hungary.

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.

No MeSH data available.


Related in: MedlinePlus