ABSTRACT
Dietary antioxidants play an important role against oxidation, an underlying mechanism in the incidence of chronic diseases. Greens+ is a commercially available preparation containing a variety of plant-derived ingredients. The aim of the current study was to evaluate the antioxidant potential of the methanolic extract of greens+ powder using in vitro and in vivo techniques. In vitro studies were conducted using a liposome model system to simulate biological cell membranes. Total antioxidant potential and polyphenol content of the herbal preparation was measured. For in vivo analysis, 10 healthy human subjects consumed either three or six teaspoons of greens+ per day for four weeks. Blood samples were analyzed at baseline and at the conclusion of the treatment period for total antioxidant capacity, polyphenol content, protein, lipid and LDL oxidation, and the level of glutathione peroxidase. Results showed that greens+ supplementation was well tolerated and increased serum antioxidant potential at higher levels of intake in a dose-dependent manner. HPLC analysis showed the presence of quercetin, apigenin, kaempferol and luteolin in the supplement. Plasma analysis indicated the presence of kaempferol only. A statistically significant (p < 0.05) reduction in protein and lipid oxidation was observed. Based on its antioxidant properties, the results suggest that greens+ might play a role in reducing the risk of chronic diseases involving a burden of oxidative damage.
Subject(s)
Antioxidants/pharmacology , Dietary Supplements , Plant Extracts/pharmacology , Adult , Antioxidants/administration & dosage , Antioxidants/chemistry , Blood Pressure/drug effects , Body Mass Index , Body Weight/drug effects , Dose-Response Relationship, Drug , Erythrocytes/drug effects , Erythrocytes/enzymology , Female , Glutathione Peroxidase/metabolism , Humans , Lipid Metabolism/drug effects , Lipid Peroxidation/drug effects , Male , Oxidation-Reduction/drug effects , Plant Extracts/administration & dosage , Plant Extracts/chemistry , Polyphenols , Proteins/metabolismABSTRACT
Stress-activated systems and oxidative stress are involved in insulin resistance, which, along with beta-cell failure, contribute to the development of type 2 diabetes mellitus (T2DM). Exercise improves insulin resistance and glucose tolerance, and these adaptations may, in part, be related to reductions in inflammation and oxidative stress. We investigated circulating and tissue-specific markers of inflammation and oxidative stress and insulin-signaling pathways in a rodent model of T2DM, the Zucker diabetic fatty rat, with and without voluntary exercise. At 5 wk of age, Zucker diabetic fatty rats (n = 8-9/group) were divided into basal (B), voluntary exercise (E), and sedentary control (S) groups. B rats were euthanized at 6 wk of age, and S and E rats were euthanized 10 wk later. E rats ran approximately 5 km/day, which improved insulin sensitivity and maintained fed and fasted glucose levels and glucose tolerance. Ten weeks of exercise also decreased whole body markers of inflammation and oxidative stress in plasma and liver, including lowered circulating IL-6, haptoglobin, and malondialdehyde levels, hepatic protein oxidation, and phosphorylated JNK, the latter indicating decreased JNK activity. Hepatic phosphoenolpyruvate carboxykinase levels and Ser(307)-phosphorylated insulin receptor substrate-1 were also reduced in E compared with S rats. In summary, we show that, in a rodent model of T2DM, voluntary exercise decreases circulating markers of inflammation and oxidative stress and lowers hepatic JNK activation and Ser(307)-phosphorylated insulin receptor substrate-1. These changes in oxidative stress markers and inflammation are associated with decreased hyperglycemia and insulin resistance and reduced expression of the main gluconeogenic enzyme phosphoenolpyruvate carboxykinase.
Subject(s)
Diabetes Mellitus, Type 2/metabolism , Diabetes Mellitus, Type 2/prevention & control , Exercise Therapy/methods , Glucose/metabolism , Insulin Receptor Substrate Proteins/metabolism , JNK Mitogen-Activated Protein Kinases/metabolism , Liver/metabolism , Animals , Disease Models, Animal , Enzyme Activation , Humans , Male , Oxidative Stress , Phosphorylation , Physical Conditioning, Animal/methods , Rats , Rats, Zucker , Serine/metabolismABSTRACT
Coronary heart disease (CHD) is a major cause of death worldwide. Dietary factors have an important role in influencing the outcome of this disease. Dietary guidelines around the world now recommend increased consumption of plant foods for the prevention of CHD. Epidemiologic and human intervention studies have documented an inverse relationship between the consumption of plant-based diets and deaths attributed to heart disease. Plant foods contain many beneficial compounds that, by acting through multiple mechanisms, provide protection against the disease. American and Canadian recommendations for the daily intake of fruits and vegetables provide a sound basis for a healthy diet and the prevention of CHD.
