This study was designed to evaluate impact of kinds of dietary grain and dietary lipid level on the glucose metabolism and antithrombogenic capacity in obesity induced rats. Total of 80 Sprague-Dawley male rats were raised for one month with control diet containing 50% (w/w) well-milled rice powder and 20% (w/w) of dietary lipids. The rats were blocked into 8 groups and raised for two months with diets containing well-milled rice, brown rice, black rice, or glutinous barley powder and 8 or 20% (w/w) of dietary lipids. The contents of total dietary fiber in experimental grains were in following order; glutinous barley > black rice > brown rice > well-milled rice. Weekly food intake were lower in glutinous barley group among all experimental groups. Body weight gain was high in high level of fat groups (20% w/w) than medium level of fat groups (8% w/w). Plasma glucose concentration was not different significantly in each groups. But brown rice group was a little lower than others. Plasma insulin concentration was lower in black rice and glutinous barley group than rice group. Plasma glucagon concentration did not differ significantly among all experimental groups. Hexokinase activities in skeletal muscle are different significantly according to level of dietary fat and grain variety factors. Brown rice group was significantly highest among all experimental groups in hexokinase activity. Plasma TXB2 concentrations in black rice and glutinous barley groups were lower as compared to rice and brown rice groups. Plasma 6-keto-PGF1alpha concentrations in glutinous barley group was higher as compared to others. In conclusion brown rice has a little lowering effect glucose concentration. Black rice and glutinous barley intakes enhance antithrombogenic capacity. It is suggested that the intakes of mixed gains are recommend.
Animals ; Blood Glucose ; Body Weight ; Edible Grain* ; Diet ; Dietary Fats ; Dietary Fiber ; Eating ; Glucagon ; Glucose* ; Hexokinase ; Hordeum ; Humans ; Insulin ; Male ; Metabolism* ; Muscle, Skeletal ; Obesity* ; Plasma ; Rats* ; Rats, Sprague-Dawley

PURPOSE: There is a fair amount of evidence indicating that increased risk of obesity and insulin resistance is associated with postmenopausal state, but can be modulated by diet and exercise. In this study, we explored whether a Pueraria lobata root-based supplement containing Rehmannia glutinosa (PR) and/or aerobic treadmill exercise can modify the metabolic changes associated with estrogen deficiency. METHODS: Seventy rats were randomly assigned to the following groups for 8 weeks (n=10 per group): SHAM, sham-operated; PR0, ovariectomized (OVX) control; PR200, OVX with PR200 mg/kg B.W; PR400, OVX with PR400 mg/kg B.W; EPR0, OVX with exercise; EPR200, OVX with exercise and PR200 mg/kg B.W; EPR400, OVX with exercise and PR400 mg/kg B.W. RESULTS: OVX induced significant increases in body weight, food intake, fat mass, LDL-cholesterol, and fasting blood glucose, confirming induction of menopausal symptoms. PR supplementation or exercise significantly suppressed the above mentioned changes through different regulatory elements in adipose tissue: PR supplement upregulated adiponectin gene expression and aerobic exercise upregulated adiponectin and insulin receptor gene expression and a combination of PR supplement and aerobic exercise showed an additive effect on adiponectin gene expression. CONCLUSION: Taken together, the results of this study suggest that PR supplement has a potential to provide health benefits in OVX rats through leptin and adiponectin secretion. In addition, the data suggest that combination of exercise and PR would have additive effects on metabolic dysfunction associated with estrogen deficiency.
Adiponectin ; Adipose Tissue ; Animals ; Blood Glucose ; Body Weight ; Diet ; Eating ; Estrogens ; Exercise* ; Fasting ; Gene Expression ; Insulin Resistance ; Insurance Benefits ; Leptin ; Obesity ; Pueraria* ; Rats* ; Receptor, Insulin ; Rehmannia*

BACKGROUND/OBJECTIVES: This study investigated the antioxidant activities and hepatoprotective effects of Schisandra chinensis Baillon extract (SCE) against tert-butyl hydroperoxide (t-BHP)-induced oxidative hepatic damage in rats. MATERIALS/METHODS: Sprague-Dawley (SD) rats were pretreated with SCE (300, 600, and 1,200 mg/kg BW) or saline once daily for 14 consecutive days. On day 14, each animal, except those belonging to the normal control group, were injected with t-BHP (0.8 mmol/kg BW/i.p.), and all of the rats were sacrificed 16 h after t-BHP injection. RESULTS: Although no significant differences in AST and ALT levels were observed among the TC and SCE groups, the high-dose SCE group showed a decreasing tendency compared to the TC group. However, erythrocyte SOD activity showed a significant increase in the low-dose SCE group compared with the TC group. On the other hand, no significant differences in hepatic total glutathione (GSH) level, glutathione reductase (GR), and glutathione peroxidase (GSH-Px) activities were observed among the TC and SCE groups. Hepatic histopathological evaluation revealed that pretreatment with SCE resulted in reduced t-BHP-induced incidence of lesions, such as neutrophil infiltration, swelling of liver cells, and necrosis. In particular, treatment with a high dose of SCE resulted in induction of phase II antioxidant/detoxifying enzyme expression, such as glutathione S-transferase (GST) and glutamate-cysteine ligase catalytic subunit (GCLC). CONCLUSIONS: Based on these results, we conclude that SCE exerts protective effects against t-BHP induced oxidative hepatic damage through the reduction of neutrophil infiltration, swelling of liver cells, and necrosis. In addition, SCE regulates the gene expression of phase II antioxidant/detoxifying enzymes independent of hepatic antioxidant enzyme activity.
Animals ; Catalytic Domain ; Erythrocytes ; Gene Expression* ; Glutamate-Cysteine Ligase ; Glutathione ; Glutathione Peroxidase ; Glutathione Reductase ; Glutathione Transferase ; Hand ; Incidence ; Liver ; Necrosis ; Neutrophil Infiltration ; Rats* ; Rats, Sprague-Dawley ; Schisandra* ; tert-Butylhydroperoxide