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Cooperative anti-diabetic effects of deoxynojirimycin-polysaccharide by inhibiting glucose absorption and modulating glucose metabolism in streptozotocin-induced diabetic mice.

Li YG, Ji DF, Zhong S, Lv ZQ, Lin TB - PLoS ONE (2013)

Bottom Line: However, the mechanisms behind these effects were not fully understood.Importantly, our histopathological observations support the results of our biochemical analyses and validate the protective effects of DPM on STZ-induced damage to the pancreas.Thus, DPM has significant potential as a therapeutic agent against diabetes.

View Article: PubMed Central - PubMed

Affiliation: Sericultural Research Institute, Zhejiang Academy of Agricultural Science, Hangzhou, China.

ABSTRACT
We had previously shown that deoxynojirimycin-polysaccharide mixture (DPM) not only decreased blood glucose but also reversed the damage to pancreatic β-cells in diabetic mice, and that the anti-hyperglycemic efficacy of this combination was better than that of 1-deoxynojirimycin (DNJ) or polysachharide alone. However, the mechanisms behind these effects were not fully understood. The present study aimed to evaluate the therapeutic effects of DPM on streptozotocin (STZ)-induced diabetic symptoms and their potential mechanisms. Diabetic mice were treated with DPM (150 mg/kg body weight) for 90 days and continued to be fed without DPM for an additional 30 days. Strikingly, decrease of blood glucose levels was observed in all DPM treated diabetic mice, which persisted 30 days after cessation of DPM administration. Significant decrease of glycosylated hemoglobin and hepatic pyruvate concentrations, along with marked increase of serum insulin and hepatic glycogen levels were detected in DPM treated diabetic mice. Results of a labeled (13)C6-glucose uptake assay indicated that DPM can restrain glucose absorption. Additionally, DPM down-regulated the mRNA and protein expression of jejunal Na(+)/glucose cotransporter, Na(+)/K(+)-ATPase and glucose transporter 2, and enhanced the activities as well as mRNA and protein levels of hepatic glycolysis enzymes (glucokinase, phosphofructokinase, private kinase and pyruvate decarboxylas E1). Activity and expression of hepatic gluconeogenesis enzymes (phosphoenolpyruvate carboxykinase and glucose-6-phosphatase) were also found to be attenuated in diabetic mice treated with DPM. Purified enzyme activity assays verified that the increased activities of glucose glycolysis enzymes resulted not from their direct activation, but from the relative increase in protein expression. Importantly, our histopathological observations support the results of our biochemical analyses and validate the protective effects of DPM on STZ-induced damage to the pancreas. Thus, DPM has significant potential as a therapeutic agent against diabetes.

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Effect of DPM on STZ-induced experimental damage to the pancreas and the liver, H&E staining, magnification, ×200.(A1, 2, 3): Control pancreas; (B1, 2, 3): Diabetic mice pancreas; (C1, 2, 3): Diabetic mice+DPM (150 mg/kg b.w.) pancreas; (a): Control liver; (b): Diabetic mice liver; (c): Diabetic mice+DPM (150 mg/kg b.w.) liver.
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pone-0065892-g007: Effect of DPM on STZ-induced experimental damage to the pancreas and the liver, H&E staining, magnification, ×200.(A1, 2, 3): Control pancreas; (B1, 2, 3): Diabetic mice pancreas; (C1, 2, 3): Diabetic mice+DPM (150 mg/kg b.w.) pancreas; (a): Control liver; (b): Diabetic mice liver; (c): Diabetic mice+DPM (150 mg/kg b.w.) liver.

Mentions: Seven days after STZ treatment, sections of pancreas from normal and diabetic mice were examined (H&E, ×200, Fig. 7). A clear decrease in the area occupied by β cells and structural derangement of the pancreas was observed in STZ-induced diabetic mice, indicating that the diabetic model was successfully established in terms of both hyperglycemia and partial pancreatic injury.


Cooperative anti-diabetic effects of deoxynojirimycin-polysaccharide by inhibiting glucose absorption and modulating glucose metabolism in streptozotocin-induced diabetic mice.

Li YG, Ji DF, Zhong S, Lv ZQ, Lin TB - PLoS ONE (2013)

Effect of DPM on STZ-induced experimental damage to the pancreas and the liver, H&E staining, magnification, ×200.(A1, 2, 3): Control pancreas; (B1, 2, 3): Diabetic mice pancreas; (C1, 2, 3): Diabetic mice+DPM (150 mg/kg b.w.) pancreas; (a): Control liver; (b): Diabetic mice liver; (c): Diabetic mice+DPM (150 mg/kg b.w.) liver.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC3675047&req=5

pone-0065892-g007: Effect of DPM on STZ-induced experimental damage to the pancreas and the liver, H&E staining, magnification, ×200.(A1, 2, 3): Control pancreas; (B1, 2, 3): Diabetic mice pancreas; (C1, 2, 3): Diabetic mice+DPM (150 mg/kg b.w.) pancreas; (a): Control liver; (b): Diabetic mice liver; (c): Diabetic mice+DPM (150 mg/kg b.w.) liver.
Mentions: Seven days after STZ treatment, sections of pancreas from normal and diabetic mice were examined (H&E, ×200, Fig. 7). A clear decrease in the area occupied by β cells and structural derangement of the pancreas was observed in STZ-induced diabetic mice, indicating that the diabetic model was successfully established in terms of both hyperglycemia and partial pancreatic injury.

Bottom Line: However, the mechanisms behind these effects were not fully understood.Importantly, our histopathological observations support the results of our biochemical analyses and validate the protective effects of DPM on STZ-induced damage to the pancreas.Thus, DPM has significant potential as a therapeutic agent against diabetes.

View Article: PubMed Central - PubMed

Affiliation: Sericultural Research Institute, Zhejiang Academy of Agricultural Science, Hangzhou, China.

ABSTRACT
We had previously shown that deoxynojirimycin-polysaccharide mixture (DPM) not only decreased blood glucose but also reversed the damage to pancreatic β-cells in diabetic mice, and that the anti-hyperglycemic efficacy of this combination was better than that of 1-deoxynojirimycin (DNJ) or polysachharide alone. However, the mechanisms behind these effects were not fully understood. The present study aimed to evaluate the therapeutic effects of DPM on streptozotocin (STZ)-induced diabetic symptoms and their potential mechanisms. Diabetic mice were treated with DPM (150 mg/kg body weight) for 90 days and continued to be fed without DPM for an additional 30 days. Strikingly, decrease of blood glucose levels was observed in all DPM treated diabetic mice, which persisted 30 days after cessation of DPM administration. Significant decrease of glycosylated hemoglobin and hepatic pyruvate concentrations, along with marked increase of serum insulin and hepatic glycogen levels were detected in DPM treated diabetic mice. Results of a labeled (13)C6-glucose uptake assay indicated that DPM can restrain glucose absorption. Additionally, DPM down-regulated the mRNA and protein expression of jejunal Na(+)/glucose cotransporter, Na(+)/K(+)-ATPase and glucose transporter 2, and enhanced the activities as well as mRNA and protein levels of hepatic glycolysis enzymes (glucokinase, phosphofructokinase, private kinase and pyruvate decarboxylas E1). Activity and expression of hepatic gluconeogenesis enzymes (phosphoenolpyruvate carboxykinase and glucose-6-phosphatase) were also found to be attenuated in diabetic mice treated with DPM. Purified enzyme activity assays verified that the increased activities of glucose glycolysis enzymes resulted not from their direct activation, but from the relative increase in protein expression. Importantly, our histopathological observations support the results of our biochemical analyses and validate the protective effects of DPM on STZ-induced damage to the pancreas. Thus, DPM has significant potential as a therapeutic agent against diabetes.

Show MeSH
Related in: MedlinePlus