scholarly journals Effects of low-volume walking programme and vitamin E supplementation on oxidative damage and health-related variables in healthy older adults

2013 ◽  
Vol 10 (1) ◽  
pp. 38 ◽  
Author(s):  
Jong-Hwan Park ◽  
Masashi Miyashita ◽  
Masaki Takahashi ◽  
Noriaki Kawanishi ◽  
Seong-Ryu Bae ◽  
...  
2010 ◽  
Vol 105 (9) ◽  
pp. 1311-1319 ◽  
Author(s):  
Ya-Fan Chiang ◽  
Huey-Mei Shaw ◽  
Mei-Fang Yang ◽  
Chih-Yang Huang ◽  
Cheng-Hsien Hsieh ◽  
...  

We previously reported that, in rodents, a diet with a high oxidised frying oil (OFO) content leads to glucose intolerance associated with a reduction in insulin secretion. The present study aimed at investigating the impairment of pancreatic islets caused by dietary OFO. C57BL/6J mice were divided into three groups to receive a low-fat basal diet containing 5 g/100 g of fresh soyabean oil (LF group) or a high-fat diet containing 20 g/100 g of either fresh soyabean oil (HF group) or OFO (HO group). After 8 weeks, mice in the HO group showed glucose intolerance and hypoinsulinaemia, and their islets showed impaired glucose-stimulated insulin secretion (P < 0·05; HO group v. LF and HF groups). Significantly higher oxidative stress and a lower mitochondrial membrane potential were observed in the islets in the HO group compared with the LF and HF groups. Immunoblots showed that the reduction in insulin levels in HO islets was associated with activation of the c-Jun NH2-terminal kinase and a reduction in levels of pancreatic and duodenal homeobox factor-1. In a second study, when dietary OFO-induced tissue vitamin E depletion was prevented by large-dose vitamin E supplementation (500 IU(1·06 mmol all-rac-α-tocopherol acetate)/kg diet; HO+E group), the OFO-mediated reduction in islet size and impairment of glucose tolerance and insulin secretion were significantly attenuated (P < 0·05; HO group v. HO+E group). We conclude that a high level of dietary OFO ingestion impairs glucose metabolism by causing oxidative damage and compromising insulin secretion in pancreatic islets, and that these effects can be prevented by vitamin E supplementation.


Clinics ◽  
2019 ◽  
Vol 74 ◽  
Author(s):  
Siti Madiani Abdul Ghani ◽  
Jo Aan Goon ◽  
Nor Helwa Ezzah Nor Azman ◽  
Siti Nor Asyikin Zakaria ◽  
Zalina Hamid ◽  
...  

Nutrients ◽  
2019 ◽  
Vol 11 (12) ◽  
pp. 2900 ◽  
Author(s):  
Gaetana Napolitano ◽  
Gianluca Fasciolo ◽  
Sergio Di Meo ◽  
Paola Venditti

Mitochondria are both the main sites of production and the main target of reactive oxygen species (ROS). This can lead to mitochondrial dysfunction with harmful consequences for the cells and the whole organism, resulting in metabolic and neurodegenerative disorders such as type 2 diabetes, obesity, dementia, and aging. To protect themselves from ROS, mitochondria are equipped with an efficient antioxidant system, which includes low-molecular-mass molecules and enzymes able to scavenge ROS or repair the oxidative damage. In the mitochondrial membranes, a major role is played by the lipid-soluble antioxidant vitamin E, which reacts with the peroxyl radicals faster than the molecules of polyunsaturated fatty acids, and in doing so, protects membranes from excessive oxidative damage. In the present review, we summarize the available data concerning the capacity of vitamin E supplementation to protect mitochondria from oxidative damage in hyperthyroidism, a condition that leads to increased mitochondrial ROS production and oxidative damage. Vitamin E supplementation to hyperthyroid animals limits the thyroid hormone-induced increases in mitochondrial ROS and oxidative damage. Moreover, it prevents the reduction of the high functionality components of the mitochondrial population induced by hyperthyroidism, thus preserving cell function.


Heart & Lung ◽  
2007 ◽  
Vol 36 (1) ◽  
pp. 16-24 ◽  
Author(s):  
Seongkum Heo ◽  
Debra K. Moser ◽  
Terry A. Lennie ◽  
Cheryl Hoyt Zambroski ◽  
Misook L. Chung

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Tomas Vetrovsky ◽  
Dan Omcirk ◽  
Jan Malecek ◽  
Petr Stastny ◽  
Michal Steffl ◽  
...  

Abstract Background Exercise training is crucial for maintaining physical and mental health in aging populations. However, as people participate in structured exercise training, they tend to behaviorally compensate by decreasing their non-exercise physical activity, thus potentially blunting the benefits of the training program. Furthermore, physical activity of older adults is substantially influenced by physical feelings such as fatigue. Nevertheless, how older people react to day-to-day fluctuations of fatigue and whether fatigue plays a role in non-exercise physical activity compensation is not known. Thus, the purpose of this study was twofold: (1) To explore whether the volume and intensity of habitual physical activity in older adults were affected by morning fatigue. (2) To investigate the effect of attending power and resistance exercise sessions on the levels of non-exercise physical activity later that day and the following day. Methods Twenty-eight older adults wore an accelerometer during a 4-week low-volume, low-intensity resistance and power training program with three exercise sessions per week and for 3 weeks preceding and 1 week following the program. During the same period, the participants were prompted every morning, using text messages, to rate their momentary fatigue on a scale from 0 to 10. Results Greater morning fatigue was associated with lower volume (p = 0.002) and intensity (p = 0.017) of daily physical activity. Specifically, one point greater on the fatigue scale was associated with 3.2 min (SE 1.0) less moderate-to-vigorous physical activity. Furthermore, attending an exercise session was associated with less moderate-to-vigorous physical activity later that day by 3.7 min (SE 1.9, p = 0.049) compared to days without an exercise session. During the next day, the volume of physical activity was greater, but only in participants with a body mass index up to 23 (p = 0.008). Conclusions Following low-volume exercise sessions, fit and healthy older adults decreased their non-exercise physical activity later that day, but this compensation did not carry over into the next day. As momentary morning fatigue negatively affects daily physical activity, we suggest that the state level of fatigue should be monitored during intensive exercise programs, especially in less fit older adults with increased fatigability.


1993 ◽  
Vol 264 (5) ◽  
pp. R992-R998 ◽  
Author(s):  
M. Meydani ◽  
W. J. Evans ◽  
G. Handelman ◽  
L. Biddle ◽  
R. A. Fielding ◽  
...  

The protective effect of vitamin E supplementation on exercise-induced oxidative damage was tested in 21 male volunteers. Nine young (22-29 yr) and 12 older (55-74 yr) sedentary male subjects participated in a double-blind protocol and received either 800 IU dl-alpha-tocopherol or a placebo daily. After 48 days, vitamin E supplementation significantly increased alpha-tocopherol in plasma and skeletal muscle. Subjects then performed a bout of eccentric exercise at 75% of their maximum heart rate by running down an inclined treadmill for 45 min. All vitamin E-supplemented subjects excreted less (P < 0.05) urinary thiobarbituric acid adducts after the exercise bout than placebo subjects at 12 days postexercise (35 and 18% above baseline in young and old supplemented groups, respectively, vs. 60 and 80% in young and old placebo groups, respectively). After exercise, the initial difference in alpha-tocopherol concentration of muscle between young placebo and vitamin E-supplemented groups was diminished and muscle lipid conjugated dienes tended to increase (P = 0.09) in placebo subjects. Placebo subjects had a significant decrease in major fatty acids of muscle biopsy taken immediately after exercise. When normalized for the hemoconcentration effects of exercise, the plasma concentration of vitamins E and C and uric acid showed no significant change. The alterations in fatty acid composition, vitamin E, and lipid conjugated dienes in muscle and in urinary lipid peroxides in controls after eccentric exercise are consistent with the concept that vitamin E provides protection against exercise-induced oxidative injury.


2015 ◽  
Vol 61 (2) ◽  
pp. 113-122 ◽  
Author(s):  
Yoshiji OHTA ◽  
Koji YASHIRO ◽  
Koji OHASHI ◽  
Yosuke HORIKOSHI ◽  
Chiaki KUSUMOTO ◽  
...  

2013 ◽  
Vol 59 (5) ◽  
pp. 375-383 ◽  
Author(s):  
Masaki TAKAHASHI ◽  
Masashi MIYASHITA ◽  
Jong-Hwan PARK ◽  
Noriaki KAWANISHI ◽  
Seong-ryu BAE ◽  
...  

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