The levels of cellular glutathione (GSH) and reactive oxygen species (ROS) simultaneously determined by fluorometric measurement, may provide important information on pro-oxidative and antioxidative balance. The dual effect of quercetin antioxidant and pro-oxidant activity was proposed from different studies. Our study demonstrated that quercetin acted as an antioxidant in HepG2 cells when cells were treated with 10 and 100 micromol/L quercetin for 30 min, but quercetin acted as a pro-oxidant when cells were incubated at 100 micromol/L quercetin for longer periods (12 and 24 h). Quercetin is capable of reducing H(2)O(2)-induced oxidative stress of HepG2 cells through different mechanisms, such as detoxification of H(2)O(2,) inhibition of ROS generation, and removal of generated ROS. We find that quercetin can block ROS generation through Fenton reaction to produce hydroxyl radicals by chelating with transition metal ions such as Cu(2+). Evidence that quercetin might exert an antioxidant effect by changing generated ROS into less reactive ROS suggests that when quercetin reacts with ROS, it becomes oxidized, which is less harmful but still reactive, and the oxidized quercetin interacts with thiol compounds as reduced GSH to return to the parent compound quercetin. In contrast, the prolonged treatment of quercetin in high concentrations (100 micromol/L) shows that quercetin may act as a pro-oxidant rather than as an antioxidant, resulting in cell death (apoptosis).

Mulberry (Morus alba L.) leaf extract (MLE) was investigated as a potent plant-derived α-glucosidase inhibitor with low α-amylase inhibitory activity. MLE was prepared by heating in an autoclave at 121 °C for 15 minutes, and its in vitro and in vivo antihyperglycemic activities were investigated. The adverse side effects of MLE were analyzed by measuring the weight and volume of the cecum, stool color, starch content in the cecum, and the integrity of intestinal transporting capacity. The in vitro inhibitory activity of MLE on intestinal α-glucosidase was potent and that on intestinal α-amylase was very weak compared with acarbose. Sugar loading tests with starch, maltose, and sucrose showed that MLE may reduce postprandial increases in blood glucose by acting as an intestinal α-glucosidase inhibitor. Feeding tests suggested that MLE may exhibit fewer adverse side effects than other α-glucosidase inhibitors, such as abdominal flatulence and meteorism, which are attributed to the impaired digestion of starch by strong inhibition of intestinal α-amylase. These results suggest that MLE could be used in the development of pharmaceutical foods to control the blood glucose levels of diabetic patients by inhibiting intestinal α-glucosidase with reduced side effects.

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The information presented might be used for developing mulberry leaf-based functional foods.

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Pancreatic lipase is the enzyme responsible for digestion and absorption of triglycerides, being its inhibition one of the widest studied methods used to determine the potential activity of natural products to inhibit dietary fat absorption. Decrease of energy intake from dietary fat through inhibition of this enzyme may be an excellent strategy to prevent and treat obesity. The inhibitory activity on pancreatic lipase enzyme of Diospyros kaki fruit and Citrus unshiu peel mixture extract (PCM) was evaluated in vitro and its antiobesity effects were studied based on the serum lipid parameters analysis from high-fat diet- (HFD-) fed mice in vivo. PCM was orally administered at a dose of 50 and 200 mg/kg body weight for 6 weeks. In addition, the activity of pancreatic lipase was assessed using orlistat (positive control). PCM exhibited inhibitory effect on lipase activity with IC50 value of 507.01 μg/mL. Moreover, serum triacylglycerol, total cholesterol levels, and visceral fat weight were significantly reduced compared to HFD control mice in PCM 200 mg/kg-treated mice (p < 0.05). These results suggest that PCM administration may be a novel potential antiobesity agent for reduction of fat absorption via inhibition of pancreatic lipase.

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