• 대한생식의학회:학술대회논문집
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• 2001.06a
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• pp.81-81
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• 2001

• Journal of Korean Biological Nursing Science
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• v.22 no.2
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• pp.139-147
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• 2020

Purpose: The purpose of this study was to determine the effects of different intensity of aerobic exercise for four weeks on cardiovascular risk factors, reactive oxygen, and antioxidant enzymes in old mice. Methods: Eighteen male C57BL/6 mice age 18 months were randomly classified into the control group (n= 6), the moderate intensity exercise group (n= 6), and the low intensity exercise group (n= 6). The training groups performed the aerobic exercise twice daily for 20 minutes, five days weekly for four weeks. Data were analyzed using descriptive statistics, analysis of variance (ANOVA), the Chi-square test, and the Tukey's test with the SPSSWIN 21.0 program. Results: In this study, among the risk factors of cardiovascular disease, blood sugar (BS) (p= .023) and total cholesterol (TC) (p= .001) were significantly different between the moderate intensity exercise group and the control group. Additionally, there were significant differences in the reactive oxygen malondialdehyde (MDA) (p= .001), the antioxidant enzymes superoxide dismutase (SOD) (p< .001) and glutathione reductase (GR) (p= .015) between the moderate intensity exercise group and the control group. Conclusion: This finding suggests that moderate intensity aerobic exercise promotes the activity of antioxidant enzymes and lowers cardiovascular risk factors in older mice.

• Journal of Life Science
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• v.20 no.7
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• pp.1012-1018
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• 2010

The aim of this study was to determine whether Alzheimer's amyloid precursor protein (APP) is dysregulated in adipose tissues of C57BL/6 male mice by high-fat diet (HFD) induced obesity, aging, or streptozotocin (STZ)-induced diabetes. APP mRNA expression was examined by quantitative real-time PCR (QPCR) in subcutaneous (SAT) and epididymal adipose tissues (EAT) from mice in 8 different condition groups. By combining conditions of age (16 weeks/26 weeks of age), diet (normal diet (ND)/high-fat diet), and induction of diabetes (non-diabetic/diabetic), 88 mice were divided into 8 different groups. QPCR demonstrated that APP expression in SAT was significantly increased by about two-fold in HFD-induced obese mice compared to both 16 week-old and 26 week-old mice in the ND group (16 weeks p=0.001; 26 weeks p<0.0001), but no changes in EAT was found. Particular effects of aging on APP gene expression were not observed in either adipose tissue depots. Significantly decreased APP expression was found in SAT in STZ-induced diabetic mice fed on ND or HFD at 16 weeks of age (ND p<0.05; HFD p<0.01). Linear regression analysis demonstrated that APP expression levels correlated with body weight in both the non-diabetic group (R=0.657, p<0.0001, n=39) and the diabetic group (R=0.508, p=<0.0001, n=49), but did not correlate with plasma glucose levels, which suggests that decreased APP expression in STZ-induced diabetic mice is most likely due to weight loss rather than hyperglycemia. These data confirm APP dysregulation by weight changes in humans and suggest a possible role linking midlife obesity with the later development of amyloidogenesis in the brain of older patients with Alzheimer's disease.

• Journal of Life Science
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• v.18 no.6
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• pp.796-803
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• 2008

Mutations in the APP gene lead to enhanced cleavage by ${\beta}-$ and ${\gamma}-secretase$, and increased $A{\beta}$ formation, which are closely associated with Alzheimer's disease (AD)-like neuropathological changes. Recent studies have shown that exercise training can ameliorate pathogenic phenotypes ($A{\beta}-42$, BDNF, GLUT-1 and HSP70) in experimental models of Alzheimer's disease. Here, we have used NSE/APPsw transgenic mice to investigate directly whether exercise training ameliorates pathogenic phenotypes within Alzheimer's brains. Sixteen weeks of exercise training resulted in a reduction of $A{\beta}-42$ peptides and also facilitated improvement of cognitive function. Furthermore, GLUT -1 and BDNF proteins produced by exercise training may protect brain neurons by inducing the concomitant expression of genes that encode proteins (HSP-70) which suppress stress induced neuron cell damages from APPsw transgenic mice. Thus, the improved cognitive function by exercise training may be mechanistically linked to a reduction of $A{\beta}-42$ peptides, possibly via activation of BDNF, GLUT-1, and HSP-70 proteins. On the basis of the evidences presented in this study, exercise training may represent a practical therapeutic management strategy for human subjects suffering from Alzheimer's disease.