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Doenjang, a Korean fermented soy food, exerts antiobesity and antioxidative activities in overweight subjects with the PPAR-γ2 C1431T polymorphism: 12-week, double-blind randomized clinical trial.
Cha, YS, Park, Y, Lee, M, Chae, SW, Park, K, Kim, Y, Lee, HS
Journal of medicinal food. 2014;(1):119-27
Abstract
We examined the antiobesity and antioxidant effects of supplementation with doenjang, a fermented soybean paste, in overweight Koreans with the PPAR-γ2 C1431T polymorphism. Sixty overweight subjects were randomly assigned to consume either 9.8 g/day of doenjang or placebo for 12 weeks. Before and after the intervention, anthropometric and metabolic parameters, along with abdominal fat distribution and PPAR-γ2 polymorphisms, were measured. Fifty-one subjects completed the study, doenjang (n=26) and placebo (n=25) groups. Relative frequencies of the PPAR-γ2 genotypes CC, TC, and TT were 70% (n=41), 25.9% (15), and 3.4% (2), whereas those of the PPAR-γ2 alleles C and T were 81.6% and 18.4%. Visceral fat area (VFA) was significantly decreased by doenjang supplementation in subjects with a mutant T allele of PPAR-γ2 compared to those with a C allele after adjusting for age, sex, and body mass index. Plasma free fatty acid, insulin, and homeostatic model assessment insulin resistance (HOMA-IR) levels were also significantly increased in the doenjang group. Doenjang pills significantly activated radical clearance capacity (ORAC and DNA tail length) in subjects with the C allele. The catalase (CAT) activity was increased twofold in the doenjang-treated group with the C allele, but this phenomenon was reversed in those with the T allele. Doenjang-treated subjects tended to have low dietary carbohydrate and sodium intakes compared with those given placebo. We found that doenjang supplementation decreased visceral fat accumulation and aging most effectively in subjects with PPAR-γ polymorphisms. This study suggests that doenjang has antiobesity and antioxidative effects in overweight individuals with mutant alleles of PPAR-γ2.
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Antioxidant enzymes induced by repeated intake of excess energy in the form of high-fat, high-carbohydrate meals are not sufficient to block oxidative stress in healthy lean individuals.
Lim, S, Won, H, Kim, Y, Jang, M, Jyothi, KR, Kim, Y, Dandona, P, Ha, J, Kim, SS
The British journal of nutrition. 2011;(10):1544-51
Abstract
It has been reported that high-fat, high-carbohydrate (HFHC) meals increase oxidative stress and inflammation. We examined whether repeated intake of excess energy in the form of HFHC meals alters reactive oxygen species (ROS) generation and the expression levels of antioxidant enzymes and mitochondrial proteins in mononuclear cells, and to determine whether this is associated with insulin resistance. We recruited healthy lean individuals (n 10). The individuals were divided into two groups: one group (n 5) ingested 10878·4 kJ/d (2600 kcal/d; 55-70 % carbohydrate, 9·5-16 % fat, 7-20 % protein) recommended by the Dietary Reference Intake for Koreans for 4 d and the other group (n 5) ingested a HFHC meal containing 14 644 kJ/d (3500 kcal/d). Then, measurements of blood insulin and glucose levels, together with suppressor of cytokine signalling-3 (SOCS-3) expression levels, were performed in both groups. Also, cellular and mitochondrial ROS levels as well as malondialdehyde (MDA) levels were measured. Expression levels of cytosolic and mitochondrial antioxidant enzymes, and mitochondrial complex proteins were analysed. Repeated intake of HFHC meals induced an increase in homeostasis model of assessment-insulin resistance (HOMA-IR), together with an increase in SOCS-3 expression levels. While a single intake of the HFHC meal increased cytosolic and mitochondrial ROS, repeated intake of HFHC meals reduced them and increased the levels of MDA, cytosolic and mitochondrial antioxidant enzymes, and several mitochondrial complex proteins. Repeated intake of HFHC meals induced cellular antioxidant mechanisms, which in turn increased lipid peroxidation (MDA) and SOCS-3 expression levels, induced hyperinsulinaemia and increased HOMA-IR, an index of insulin resistance. In conclusion, excess energy added to a diet can generate detrimental effects in a short period.
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β-Carotene and lutein inhibit hydrogen peroxide-induced activation of NF-κB and IL-8 expression in gastric epithelial AGS cells.
Kim, Y, Seo, JH, Kim, H
Journal of nutritional science and vitaminology. 2011;(3):216-23
Abstract
Reactive oxygen species (ROS) including hydrogen peroxide (H(2)O(2)) are involved in the pathogenesis of gastric inflammation. Interleukin-8 (IL-8) is a potent mediator of the inflammatory response by activating and recruiting neutrophils to the site of infection. Oxidant-sensitive transcription factor NF-κB regulates the expression of IL-8 in the immune and inflammatory events. Carotenoids (carotenes and oxygenated carotenoids) show antioxidant and anti-inflammatory activities. Low intake of β-carotene leads to high risk of gastric cancer. Oxygenated carotenoid lutein inhibited NF-κB activation in experimental uveitis. The present study aims to investigate whether β-carotene and lutein inhibit H(2)O(2)-induced activation of NF-κB and expression of IL-8 in gastric epithelial AGS cells. The cells were treated with carotenoids 2 h prior to the treatment of H(2)O(2). mRNA expression was analyzed by reverse transcription-polymerase chain reaction (RT-PCR) and real time RT-PCR analyses. IL-8 level in the medium was determined by enzyme-linked immunosorbent assay. NF-κB activation was assessed by electrophoretic mobility shift assay. ROS levels of the cells were detected by confocal microscopic analysis for fluorescent dichlorofluorescein. As a result, H(2)O(2 )induced the activation of NF-κB and expression of IL-8 in AGS cells time-dependently. β-Carotene and lutein showed inhibitory effects on H(2)O(2)-induced increase in intracellular ROS levels, activation of NF-κB, and IL-8 expression in AGS cells. In conclusion, supplementation of carotenoids such as β-carotene and lutein may be beneficial for the treatment of oxidative stress-mediated gastric inflammation.
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Effects of vitamin treatment or supplements with purported antioxidant properties on skin cancer prevention: a meta-analysis of randomized controlled trials.
Chang, YJ, Myung, SK, Chung, ST, Kim, Y, Lee, EH, Jeon, YJ, Park, CH, Seo, HG, Huh, BY
Dermatology (Basel, Switzerland). 2011;(1):36-44
Abstract
AIMS: To investigate the effect of vitamin treatment or supplements with purported antioxidant properties on the primary and secondary prevention of skin cancer using a meta-analysis of randomized controlled trials (RCTs). METHODS We searched PubMed, Embase and the Cochrane Library in June 2009. Among 398 articles searched, 11 articles on 10 RCTs were included in the final analysis. RESULTS In a fixed-effects meta-analysis of all 10 trials, vitamin treatment or supplements with purported antioxidant properties were found to have no preventive effect on skin cancer [relative risk (RR) = 0.98; 95% confidence interval (CI) = 0.94-1.03]. Similar findings were observed in a subgroup meta-analysis of 10 studies on both primary prevention trials (RR = 0.98; 95% CI = 0.93-1.03) and secondary prevention trials (RR = 0.97; 95% CI = 0.83-1.13). Further, subgroup meta-analyses revealed no preventive effect on cancer by type of antioxidant, type of cancer and the methodological quality of the studies. CONCLUSION The current meta-analysis of RCTs indicated that there is no clinical evidence to support an overall primary and secondary preventive effect of vitamin treatment or supplements with purported antioxidant properties on skin cancer. The effect of vitamin supplements on skin cancer should not be overemphasized.
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Effects of antioxidant supplements on cancer prevention: meta-analysis of randomized controlled trials.
Myung, SK, Kim, Y, Ju, W, Choi, HJ, Bae, WK
Annals of oncology : official journal of the European Society for Medical Oncology. 2010;(1):166-79
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Abstract
BACKGROUND This meta-analysis aimed to investigate the effect of antioxidant supplements on the primary and secondary prevention of cancer as reported by randomized controlled trials. METHODS We searched Medline (PubMed), Excerpta Medica database, and the Cochrane Review in October 2007. RESULTS Among 3327 articles searched, 31 articles on 22 randomized controlled trials, which included 161 045 total subjects, 88 610 in antioxidant supplement groups and 72 435 in placebo or no-intervention groups, were included in the final analyses. In a fixed-effects meta-analysis of all 22 trials, antioxidant supplements were found to have no preventive effect on cancer [relative risk (RR) 0.99; 95% confidence interval (CI) 0.96-1.03). Similar findings were observed in 12 studies on primary prevention trials (RR 1.00; 95% CI 0.97-1.04) and in nine studies on secondary prevention trials (RR 0.97; 95% CI 0.83-1.13). Further, subgroup analyses revealed no preventive effect on cancer according to type of antioxidant, type of cancer, or the methodological quality of the studies. On the other hand, the use of antioxidant supplements significantly increased the risk of bladder cancer (RR 1.52; 95% CI 1.06-2.17) in a subgroup meta-analysis of four trials. CONCLUSIONS The meta-analysis of randomized controlled trials indicated that there is no clinical evidence to support an overall primary and secondary preventive effect of antioxidant supplements on cancer. The effects of antioxidant supplements on human health, particularly in relation to cancer, should not be overemphasized because the use of those might be harmful for some cancer.