No abstract

It is suggested that the difference in the mice fed vitamin E supplemented diet is due to an increase of insulin secretion and that vitamin E supplementation may have a role in helping to slow the stages of diabetes mellitus.

Root of burdock contains high amounts of dietary fibers and polyphenols. To improve the functional properties, the root was fermented with Aspergillus awamori. Effect of the fermented burdock on alloxan-induced mouse diabetes was examined. A diet containing the 5% fermented burdock powers was prepared to examine effect of the burdock diet on alloxan-induced mouse diabetes. Mice fed the burdock diet and the control diet for 14 weeks. Then, alloxan (200 mg/kg of body weight) was administrated to each mouse. After 5 days from the administration, blood glucose assay and glucose tolerance test were carried out. Incidence of hyperglycemia decreased and the glucose metabolism was improved when mice fed the burdock diet. Insulin, C-peptide, biomarkers of oxidative stress in plasma and apoptosis in pancreas were examined and compared to those obtained from mice fed the control diet. It is deduced that alloxan-induced diabetes is caused to lower insulin concentration. The fermented-burdock diet improves the diabetes and prevents apoptosis in the pancreas.

Backgrounds:We reported that feeding 5% Asperagillus awamori-fermented burdock root diet was effective in preventing mouse hyperglycemia caused by alloxan.Methods: Diets containing 5% burdock roots were prepared from raw and Asperagillus awamori-fermented burdock root powders. Acatalasemic mice, having a quite low catalase activity in blood, and normal mice were fed these diets for 14 weeks, separately. Then, alloxan (200 mg/kg of body weight) or PBS was intraperitoneally administrated to each mouse. After 5 day from the administration, blood glucose assay and glucose tolerance test were carried out, and then insulin, C-peptide and lipid peroxide in plasma were examined.Results: Incidences of hyperglycemia in normal mice fed control, raw and fermented burdock root diets were 25, 20 and 11%, respectively, and these in acatalasemic mice were 73, 80 and 27%. Insulin and C-peptide in plasma of mice fed raw burdock root diet or control diet were low compared to mice fed the fermented diet. Conclusions:Intake of raw burdock root does not suppress the alloxan-induced hyperglycemia but the fermented burdock root does. It is suggested that Asperagillus awamori plays an important role for the prevention.

Background: Catalase deficiency (acatalasemia) is sensitive to alloxan, and the administration to acatalasemic mice develops hyperglycemia under mild conditions. However, the mechanism is still poorly understood. Methods: Alloxan was used to induce the oxidative stress and intraperitoneally administered to acatalasemic and normal mice. The blood samples of these mice after 1, 3, 5 and 7 days were examined. The pancreatic islets 7 days after alloxan administration were isolated, and the insulin released under 3 mM and 20 mM glucose was examined. Results: After alloxan administration, increase of oxidative markers in blood and pancreatic apoptosis in acatalasemic mice were observed immediately. Insulin in blood was lowered after 3 days, and the insulin in acatalasemic mice was lower than that in normal mice. Hyperglycemia in the acatalasemic mice was observed after 3 days. The pancreatic islets after 7 days were isolated. A reduction of the insulin released from the islets under glucose stimulation was observed. The stimulation indexes of the normal and acatalasemic mice were 1.4 ± 0.6 and 0.7 ± 0.3, respectively. Conclusions: Alloxan induced a deterioration of glucose-dependent insulin secretion ability from the islets, and the deterioration mostly contributed to hyperglycemia, rather than apoptosis.

The reactive oxygen species generated with alloxan and reducing agents in the body selectively injure β‐cells in the pancreas so as to cause diabetes. As alloxan generated hydrogen peroxide with reduced glutathione, acatalasemic mice, having a quite low catalase activity in blood, became diabetic with a smaller dose than those having normal one. As the injury caused by oxidative stress is ameliorated by the intake of antioxidants, we chose vitamin E and a fermented burdock to serve as antioxidants. Effects of these diets on acatalasemic mouse diabetes caused by alloxan were examined. Mice were maintained on a control diet and one of these antioxidant diets, respectively, for 14 weeks. Alloxan was then intraperitoneally administered, and blood glucose, glucose tolerance and the insulin level in mouse blood were examined. The incidence of hyperglycemia in the mice maintained on the control diet was significantly higher than that in the mice maintained on the supplemented diet. The abnormal glucose metabolism caused by alloxan administration was ameliorated by both supplemented diets. It is deduced that these antioxidants can prevent a decrease of insulin concentration in the blood in this mouse model.