Chien-Wen Hou

Ginsenoside-Rg1 Protects the Liver against Exhaustive Exercise-Induced Oxidative Stress in Rats.

Despite regular exercise benefits, acute exhaustive exercise elicits oxidative damage in liver. The present study determined the hepatoprotective properties of ginsenoside-Rg1 against exhaustive exercise-induced oxidative stress in rats. Forty rats were assigned into vehicle and ginsenoside-Rg1 groups (0.1 mg/kg bodyweight). After 10-week treatment, ten rats from each group performed exhaustive swimming. Estimated oxidative damage markers, including thiobarbituric acid reactive substance (TBARS) (67%) and protein carbonyls (56%), were significantly (P < 0.01) elevated after exhaustive exercise but alleviated in ginsenoside-Rg1 pretreated rats. Furthermore, exhaustive exercise drastically decreased glutathione (GSH) content (∼79%) with concurrent decreased superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px) activities. However, these changes were attenuated in Rg1 group. Additionally, increased xanthine oxidase (XO) activity and nitric oxide (NO) levels after exercise were also inhibited by Rg1 pretreatment. For the first time, our findings provide strong evidence that ginsenoside-Rg1 can protect the liver against exhaustive exercise-induced oxidative damage.

Short-term Altitude Mountain Living Improves Glycemic Control

The aim of this study was to investigate the effect of mountain living conditions and high altitude hiking activities on glucose tolerance. In study I, we performed an oral glucose tolerance test on nine untrained subjects before and after 3 days of mountain living. In study II, the same measurement was used to determine the effect of high altitude hiking in two distinct geographic environments; participants included 19 professionally trained mountaineers. We found that trained mountaineers displayed significantly better sea-level glucose tolerance than sedentary subjects of a similar age (p < 0.05). This result suggests that mountaineering training could produce a beneficial effect on glucose tolerance. More importantly, in study I we demonstrated that 3 days of high altitude living (altitude approximately 2400 m) was sufficient to improve glucose tolerance. Furthermore, hiking in a relatively flat plateau area (Pamirs highland area, China, altitude approximately 4000 m) generated significantly better improvement in glucose tolerance than hiking in a mountain that contained many rough hills at a similar altitude (Mountain Snow, Taiwan, altitude approximately 3800 m). In conclusion, we found that living at a high altitude for the short term can significantly improve glucose tolerance. Additionally, the improving effect of hiking at high altitudes on glucose tolerance appears to be influenced by the geographic environment. These preliminary results suggest that high altitude living conditions and activities may possibly be developed as potential natural medicines for the prevention and treatment of type II diabetes in the future.

Oral Rg1 supplementation strengthens antioxidant defense system against exercise-induced oxidative stress in rat skeletal muscles

BackgroundPrevious studies reported divergent results on nutraceutical actions and free radical scavenging capability of ginseng extracts. Variations in ginsenoside profile of ginseng due to different soil and cultivating season may contribute to the inconsistency. To circumvent this drawback, we assessed the effect of major ginsenoside-Rg1 (Rg1) on skeletal muscle antioxidant defense system against exhaustive exercise-induced oxidative stress.MethodsForty weight-matched rats were evenly divided into control (N = 20) and Rg1 (N = 20) groups. Rg1 was orally administered at the dose of 0.1 mg/kg bodyweight per day for 10-week. After this long-term Rg1 administration, ten rats from each group performed an exhaustive swimming, and remaining rats considered as non-exercise control. Tibialis anterior (TA) muscles were surgically collected immediately after exercise along with non-exercise rats.ResultsExhaustive exercise significantly (p<0.05) increased the lipid peroxidation of control group, as evidenced by elevated malondialdehyde (MDA) levels. The increased oxidative stress after exercise was also confirmed by decreased reduced glutathione to oxidized glutathione ratio (GSH/GSSG ratio) in control rats. However, these changes were completely eliminated in Rg1 group. Catalase (CAT) and glutathione peroxidase (GPx) activities were significantly (p<0.05) increased by Rg1 in non-exercise rats, while no significant change after exercise. Nevertheless, glutathione reductase (GR) and glutathione S-transferase (GST) activities were significantly increased after exercise in Rg1 group.ConclusionsThis study provide compelling evidences that Rg1 supplementation can strengthen antioxidant defense system in skeletal muscle and completely attenuate the membrane lipid peroxidation induced by exhaustive exercise. Our findings suggest that Rg1 can use as a nutraceutical supplement to buffer the exhaustive exercise-induced oxidative stress.

Effect of exercise training on ethanol-induced oxidative damage in aged rats

It is well known that lipid peroxidation increases with age, and alcohol drinking further exacerbates this damage. The present study determined the effect of regular exercise training on alcohol-induced oxidative damage and antioxidant status in the liver of aged animals. The age-matched Wistar albino rats (3 months young, n=24; 18 months old, n=24) were evenly divided into four groups: control (C), exercise trained (Ex), ethanol drinking (Et), and exercise plus ethanol drinking (Ex+Et). With ethanol drinking, hepatic malondialdehyde (MDA) level was significantly elevated above control (P<.001), whereas glutathione (GSH) and ascorbic acid (vitamin C) contents were significantly decreased below control. These changes were found to be greater in the aged rats than those of the young rats. For both age groups, exercise training significantly reversed the increase in MDA and decreases in GSH and ascorbic acid induced by ethanol drinking. The present study showed that ethanol-induced deterioration in lipid peroxidation and reduction in antioxidant status in the liver were exacerbated with age. Here, we found that exercise training significantly reversed the adverse conditions that were caused by ethanol in aged rats.

Alcohol-induced deterioration in primary antioxidant and glutathione family enzymes reversed by exercise training in the liver of old rats

Chronic alcohol consumption causes severe hepatic oxidative damage, particularly to old subjects by decreasing various antioxidant enzymes. In this study, we test the hypothesis that exercise training can protect the aging liver against alcohol-induced oxidative damage. Two different age groups of Wistar albino rats (3 months young, n=24; 18 months old, n=24) were evenly divided into four groups: control (Con), exercise trained (Tr, 23 m/min 30 min/day, 5 days/week for 2 months), ethanol drinking/treated (Et, 2.0 g/kg b.w. orally), and exercise training plus ethanol drinking/treated (Tr+Et). We found significantly (P<.001) lowered hepatic antioxidant enzymes including superoxide dismutase, catalase, selenium (Se)-dependent glutathione peroxidase (Se-GSH-Px), Se-non-dependent glutathione peroxidase (non-Se-GSH-Px), glutathione reductase, and glutathione S-transferase activities in aged rats compared with young. Age-related decrease in antioxidant enzyme status was further exacerbated with ethanol drinking, which indicates liver in aged rats is more susceptible to oxidative damage because of decreased free radical scavenging system in aged/old ethanol-drinking rats. However, the decrease in liver antioxidant enzymes status with ethanol consumption was ameliorated by 2 months exercise training in old and young rats. These results demonstrate that age-associated decrease in hepatic free radical scavenging system exacerbated by ethanol drinking. For the first time, we found that this deterioration was significantly reversed by exercise training in aging liver, thus protects against alcohol-induced oxidative damage.

Deep ocean mineral water accelerates recovery from physical fatigue

BackgroundDeep oceans have been suggested as a possible site where the origin of life occurred. Along with this theoretical lineage, experiments using components from deep ocean water to recreate life is underway. Here, we propose that if terrestrial organisms indeed evolved from deep oceans, supply of deep ocean mineral water (DOM) to humans, as a land creature, may replenish loss of molecular complexity associated with evolutionary sea-to-land migration.MethodsWe conducted a randomized, double-blind, placebo-controlled crossover human study to evaluate the effect of DOM, taken from a depth of 662 meters off the coast of Hualien, Taiwan, on time of recovery from a fatiguing exercise conducted at 30°C.ResultsThe fatiguing exercise protocol caused a protracted reduction in aerobic power (reduced VO2max) for 48 h. However, DOM supplementation resulted in complete recovery of aerobic power within 4 h (P < 0.05). Muscle power was also elevated above placebo levels within 24 h of recovery (P < 0.05). Increased circulating creatine kinase (CK) and myoglobin, indicatives of exercise-induced muscle damage, were completely eliminated by DOM (P < 0.05) in parallel with attenuated oxidative damage (P < 0.05).ConclusionOur results provide compelling evidence that DOM contains soluble elements, which can increase human recovery following an exhaustive physical challenge.

Altitude Hypoxia Increases Glucose Uptake in Human Heart

Chen, Chi-Hsien, Yuh-Feng Liu, Shin-Da Lee, Wen-Chih Lee, Ying-Lan Tsai, Chien-Wen Hou, Chih-Yang Huang, and Chia-Hua Kuo. Altitude hypoxia increases glucose uptake in human heart. High Alt. Med Biol. 10:83-86, 2009.-Cardiac muscle is a highly oxygenated tissue that produces ATP mainly from fat oxidation. However, when the rate of oxygen demand exceeds oxygen supply, energy reliance on the carbohydrate substrate becomes crucial for sustaining normal cardiac function. In this study, the effect of acute altitude hypoxia on glucose uptake from circulation was determined, for the first time, in the human heart, using [18F]-2-deoxy-2-fluoro-D-glucose positron emission tomography (FDG-PET) in a simulated altitude condition (14% O(2), corresponding to approximately 3000 m above sea level) or room air (21% O(2)). Our results showed that subjects (n = 6) started to experience difficulty in sustaining the hypoxic condition at approximately 45 min. This was concurrent with a substantially increased blood lactate concentration, which reflects an accelerated rate of anaerobic glycolysis. Hypoxia elevated FDG uptake above control by approximately 70% in heart, but not in limbs (representing primarily skeletal muscle), brain, and liver. This study provides the first human evidence for the hypoxia-stimulated glucose uptake in heart. At this hypoxia level, the previously observed hypoxia-stimulated glucose uptake in rat skeletal muscle was not confirmed in the human study.

Physiological Effects of Bioceramic Material: Harvard Step, Resting Metabolic Rate and Treadmill Running Assessments

Previous biomolecular and animal studies have shown that a room-temperature far-infrared-rayemitting ceramic material (bioceramic) demonstrates physical-biological effects, including the normalization of psychologically induced stress-conditioned elevated heart rate in animals. In this clinical study, the Harvard step test, the resting metabolic rate (RMR) assessment and the treadmill running test were conducted to evaluate possible physiological effects of the bioceramic material in human patients. The analysis of heart rate variability (HRV) during the Harvard step test indicated that the bioceramic material significantly increased the high-frequency (HF) power spectrum. In addition, the results of RMR analysis suggest that the bioceramic material reduced oxygen consumption (VO2). Our results demonstrate that the bioceramic material has the tendency to stimulate parasympathetic responses, which may reduce resting energy expenditure and improve cardiorespiratory recovery following exercise.

Interactive Effect of Exercise Training and Growth Hormone Administration on Glucose Tolerance and Muscle GLUT4 Protein Expression in Rats

The insulin-resistance effect of growth hormone (GH) administration has been frequently reported. The present study investigated the effect of GH administration on glucose tolerance and muscle GLUT4 protein expression in exercise-trained and untrained rats. Forty-eight rats were weight-matched and assigned to the following 4 groups: control, GH, exercise training, and exercise training + GH groups. After 2 weeks of GH injections (65 µg/kg/day) and exercise training, the glucose tolerance and insulin response were measured in these rats. The GLUT4 protein level, glycogen storage, and citrate synthase activity were determined in red gastrocnemius and plantaris muscles. Daily GH administration elevated the curves of the oral glucose tolerance test and insulin response compared with those of saline-injected control rats. Furthermore, exercise training completely eliminated this GH-induced insulin resistance as determined 18 h after the last bout of exercise training. Additionally, exercise training significantly increased muscle glycogen storage and GLUT4 protein levels. GH administration did not affect the GLUT4 protein and glycogen storage increases induced by exercise training, but the citrate synthase activity in the plantaris muscle was further elevated by GH administration to a level above that induced by training. In conclusion, this is the first study that demonstrates that regular exercise training prevents GH-induced insulin-resistance side effect in rats.

Effect of Black Soybean Koji Extract on Glucose Utilization and Adipocyte Differentiation in 3T3-L1 Cells

Adipocyte differentiation and the extent of subsequent fat accumulation are closely related to the occurrence and progression of diseases such as insulin resistance and obesity. Black soybean koji (BSK) is produced by the fermentation of black soybean with Aspergilllus awamori. Previous study indicated that BSK extract has antioxidative and multifunctional bioactivities, however, the role of BSK in the regulation of energy metabolism is still unclear. We aimed to investigate the effect of glucose utilization on insulin-resistant 3T3-L1 preadipocytes and adipogenesis-related protein expression in differentiated adipocytes with BSK treatment. Cytoxicity assay revealed that BSK did not adversely affect cell viability at levels up to 200 μg/mL. The potential for glucose utilization was increased by increased glucose transporter 1 (GLUT1), GLUT4 and protein kinase B (AKT) protein expression in insulin-resistant 3T3-L1 cells in response to BSK treatment. Simultaneously, BSK inhibited lipid droplet accumulation in differentiated 3T3-L1 cells. The inhibitory effect of adipogenesis was associated with downregulated peroxisome proliferator-activated receptor γ (PPARγ) level and upregulated Acrp30 protein expression. Our results suggest that BSK extract could improve glucose uptake by modulating GLUT1 and GLUT4 expression in a 3T3-L1 insulin-resistance cell model. In addition, BSK suppressed differentiation and lipid accumulation in mature 3T3-L1 adipocytes, which may suggest its potential for food supplementation to prevent obesity and related metabolic abnormalities.