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1.
China Journal of Chinese Materia Medica ; (24): 1194-1198, 2007.
Article in Chinese | WPRIM | ID: wpr-235235

ABSTRACT

<p><b>OBJECTIVE</b>To study the hypoglycemic effect of the extract of B. polyandra (SHG).</p><p><b>METHOD</b>The diabetic mice were induced by alloxan in ICR mice. The blood glucose concentration was measured by glucose oxidase method. The serum insulin level was determined by 125I-insulin radioimmunoassay kit. The hypoglycemic effect was evaluated by the levels of both fasting and no-fasting blood glucose. The effect on serum insulin level was estimated by the values of the blood insulin and the changes of the blood glucose induced by the glucose intraperitoneal injection. The effect on the glucose absorption was investigated by the oral sucrose or starch tolerance test.</p><p><b>RESULT</b>Both of the fasting and no-fasting blood glucose levels were decreased significantly by the treatment of 20 or 30 g raw materials crude drug x kg (-1) SHG orally for 7-10 d in ICR mice or in alloxan diabetic mice. In the oral sucrose tolerance test or oral starch tolerance test, the administration of SHG reduced significantly the peak value of the blood glucose and the area under the blood glucose-time curve (AUC) in normal or alloxan diabetic mice, respectively. These effects of SHG were similar to those of acarbose, a kind of alpha-glucosidase inhibitors. In the oral glucose tolerance test in normal and alloxan diabetic mice, SHG decreased both the blood glucose peak and the AUC induced by the glucose loading. But in the intraperitoneal injection glucose tolerance test the levels of insulin in both SHG and control mice were similar, however, the changes of the blood glucose level after the glucose-loading for 30 min in SHG mice was much lower than that in control mice.</p><p><b>CONCLUSION</b>With the treatment of SHG, the fasting and no-fasting blood glucose concentrations were decreased and the glucose tolerance improved significantly in both normal and alloxan diabetic mice, and the inhibition of a-glucosidase might be one of its major mechanisms.</p>


Subject(s)
Animals , Male , Mice , Administration, Oral , Alloxan , Area Under Curve , Blood Glucose , Diabetes Mellitus, Experimental , Blood , Drugs, Chinese Herbal , Pharmacology , Glucose , Pharmacokinetics , Glucose Tolerance Test , Hypoglycemic Agents , Pharmacology , Injections, Intraperitoneal , Insulin , Blood , Mice, Inbred ICR , Phytotherapy , Plants, Medicinal , Chemistry , Random Allocation , alpha-Glucosidases , Metabolism
2.
Acta Pharmaceutica Sinica ; (12): 418-422, 2005.
Article in Chinese | WPRIM | ID: wpr-353444

ABSTRACT

<p><b>AIM</b>To set up an IR-HIRc cell model for screening the inhibitor of GFAT (glutamine: fructose-6-phosphate amidotransferase) , the key enzyme in the hexosamine biosynthesis pathway (HBP).</p><p><b>METHODS</b>For GFAT activity assay, the GDH method was improved by adjusting the value of pH in the reaction system and the concentrations of the reactants. The sensitivity to insulin in the cells was estimated by the measurement of insulin-induced glucose-uptake. The IR-HIRc model was set up by the stimulation of long-action insulin for 36 h. The IR-HIRc model and GDH method was used for screening GFAT inhibitor.</p><p><b>RESULTS</b>With the administration of 25 nmol x L(-1) long-action insulin in HIRe cells for 36 hours, the GFAT activity increased by 47% and the insulin-induced glucose-uptake decreased by 21%. Azaserine, a GFAT inhibitor, inhibited GFAT activity significantly in a dose-dependent manner in IR-HIRc model.</p><p><b>CONCLUSION</b>With the stimulation of 25 nmol x L(-1) long-action insulin for 36 h, excess hexosamine flux and insulin resistant in IR-HIRc cell model was set up, which can be used for screening</p>


Subject(s)
Animals , Rats , Azaserine , Pharmacology , Cell Line , Dose-Response Relationship, Drug , Fibroblasts , Cell Biology , Metabolism , Glucose , Metabolism , Glutamine-Fructose-6-Phosphate Transaminase (Isomerizing) , Metabolism , Hexosamines , Insulin , Pharmacology , Insulin Resistance , Models, Biological , Recombinant Proteins , Metabolism
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