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The effects of endurance training on...

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The effects of endurance training on cardiac function, mitochondrial respiration and oxidative stress level in type 2 diabetic mice.

紀錄類型:	書目-語言資料,印刷品 : Monograph/item
正題名/作者:	The effects of endurance training on cardiac function, mitochondrial respiration and oxidative stress level in type 2 diabetic mice./
作者:	McCurley, Libby.
面頁冊數:	55 p.
附註:	Source: Dissertation Abstracts International, Volume: 69-05, Section: B, page: 2696.
Contained By:	Dissertation Abstracts International69-05B.
標題:	Biology, Animal Physiology. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3317828
ISBN:	9780549660811

The effects of endurance training on cardiac function, mitochondrial respiration and oxidative stress level in type 2 diabetic mice.
McCurley, Libby.

The effects of endurance training on cardiac function, mitochondrial respiration and oxidative stress level in type 2 diabetic mice. - 55 p.

Source: Dissertation Abstracts International, Volume: 69-05, Section: B, page: 2696.

Thesis (Ph.D.)--University of Arkansas, 2008.

The prevalence of type 2 diabetes is rapidly growing in our nation and throughout the world. The disease, if not controlled, greatly alters energy metabolism and frequently leads to the development of a diabetes-specific cardiomyopathy. Mitochondrial dysfunction and increased oxidative stress levels have been associated with this form of cardiomyopathy, but the relationship is not fully understood. To examine the effects of endurance training on cardiac function, mitochondrial function and oxidative stress level, 28 db/db mice and 29 control mice were used. The db/db and control mice were randomly assigned as either endurance trained (ED) or sedentary (SD) as were the non-diabetics (END) and (SND). Trained mice were run on a treadmill at 18-24 m/min, 30 minutes per day, 5 days per week for 5-8 weeks while sedentary animals received only cage activity. Body weight, glucose level and left ventricular function were assessed prior to and following training. At the end of training, animals were randomly selected from each group for final data collection. This data collection included measurement of cardiac dimensions by means of echocardiography, glucose level and heart weight measurement, and isolation of mitochondrial protein for assessment of mitochondrial respiration. Samples of cardiac whole homogenate were also collected for measurement of GSH:GSSG. All post-training data, except glucose and body weight, were analyzed using a 2(Disease State) x 2(Training State) x 2(Training Duration) factorial ANOVA with post-hoc tests where applicable. Post-training glucose and body weight were analyzed using a 2 x 2 ANCOVA with pre-training weight as the covariate. Level of significance for all analyses was set at p<.05. Results showed a significantly higher level of oxidative stress in diabetic compared to non-diabetic animals ( p=.0023). Near significant differences were observed for oxidative stress for training state (p=.0545) with trained animals exhibiting less oxidative stress than untrained animals. The post-hoc test for training duration also resulted in near significance (p=.0561) with longer training duration associated with lower oxidative stress level. Mitochondrial respiration analyses did not show significant differences, but the greatest control was seen in the short duration SND mice and the poorest control was observed for the long duration ED mice. Cardiac function as described by ejection fraction and fractional shortening was significantly better in non-diabetics compared to diabetics (p<.0001) and for trained compared to sedentary mice (p=.0210). Post-training body weight was higher in diabetic mice (p<.0001) and in sedentary mice (p<.0001) compared to non-diabetic and trained mice, respectively. Heart weights of diabetic mice were significantly lower (p<.0001) than non-diabetic mice even though diabetic body weight was much greater. Water consumption was greater in SD when compared to ED mice (p=.0003) but greater in END compared to SND mice (p=.0002). Food consumption was also greater in SD compared to ED mice (p=.0218). The findings in the present study support previous studies which show the detrimental effects of diabetes on cardiac oxidative stress level and left ventricular cardiac functioning. This research also suggests that endurance training has a protective effect against cardiac oxidative stress as well as cardiac functioning and metabolic wasting.

ISBN: 9780549660811Subjects--Topical Terms:

1017835
Biology, Animal Physiology.

The effects of endurance training on cardiac function, mitochondrial respiration and oxidative stress level in type 2 diabetic mice.
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245 1 4 $a The effects of endurance training on cardiac function, mitochondrial respiration and oxidative stress level in type 2 diabetic mice.
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502 $a Thesis (Ph.D.)--University of Arkansas, 2008.
520 $a The prevalence of type 2 diabetes is rapidly growing in our nation and throughout the world. The disease, if not controlled, greatly alters energy metabolism and frequently leads to the development of a diabetes-specific cardiomyopathy. Mitochondrial dysfunction and increased oxidative stress levels have been associated with this form of cardiomyopathy, but the relationship is not fully understood. To examine the effects of endurance training on cardiac function, mitochondrial function and oxidative stress level, 28 db/db mice and 29 control mice were used. The db/db and control mice were randomly assigned as either endurance trained (ED) or sedentary (SD) as were the non-diabetics (END) and (SND). Trained mice were run on a treadmill at 18-24 m/min, 30 minutes per day, 5 days per week for 5-8 weeks while sedentary animals received only cage activity. Body weight, glucose level and left ventricular function were assessed prior to and following training. At the end of training, animals were randomly selected from each group for final data collection. This data collection included measurement of cardiac dimensions by means of echocardiography, glucose level and heart weight measurement, and isolation of mitochondrial protein for assessment of mitochondrial respiration. Samples of cardiac whole homogenate were also collected for measurement of GSH:GSSG. All post-training data, except glucose and body weight, were analyzed using a 2(Disease State) x 2(Training State) x 2(Training Duration) factorial ANOVA with post-hoc tests where applicable. Post-training glucose and body weight were analyzed using a 2 x 2 ANCOVA with pre-training weight as the covariate. Level of significance for all analyses was set at p<.05. Results showed a significantly higher level of oxidative stress in diabetic compared to non-diabetic animals ( p=.0023). Near significant differences were observed for oxidative stress for training state (p=.0545) with trained animals exhibiting less oxidative stress than untrained animals. The post-hoc test for training duration also resulted in near significance (p=.0561) with longer training duration associated with lower oxidative stress level. Mitochondrial respiration analyses did not show significant differences, but the greatest control was seen in the short duration SND mice and the poorest control was observed for the long duration ED mice. Cardiac function as described by ejection fraction and fractional shortening was significantly better in non-diabetics compared to diabetics (p<.0001) and for trained compared to sedentary mice (p=.0210). Post-training body weight was higher in diabetic mice (p<.0001) and in sedentary mice (p<.0001) compared to non-diabetic and trained mice, respectively. Heart weights of diabetic mice were significantly lower (p<.0001) than non-diabetic mice even though diabetic body weight was much greater. Water consumption was greater in SD when compared to ED mice (p=.0003) but greater in END compared to SND mice (p=.0002). Food consumption was also greater in SD compared to ED mice (p=.0218). The findings in the present study support previous studies which show the detrimental effects of diabetes on cardiac oxidative stress level and left ventricular cardiac functioning. This research also suggests that endurance training has a protective effect against cardiac oxidative stress as well as cardiac functioning and metabolic wasting.
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