Oral Sodium Metavanadate Improves Glucose Phosphorylation In Diabetic ICR Mice

In this study, oral administration of sodium metavanadate for 5 weeks on glucose phosphorylation was investigated in diabetic ICR mice. The diabetic ICR mice were induced by alloxan. The liver glucokinase, muscle hexokinase, blood glucose and insulin were assayed. The purposes of this study were to research how sodium metavanadate affect the glucose phosphorylation in diabetic ICR mice, to observe the relationship between glucose phosphorylation and anti-hyperglycemia, to investigate the effect of sodium metavanadate to the secreting of insulin, and to deduce the mechanisms of anti-hyperglycemia of oral sodium metavanadate.We chose the ICR mice as objects of study. They were all female , and about 28 + 2 grams before the experiment .We randomly allocated them into induced diabetic group and control group. The induced diabetic group was given alloxanintraperitoneally. The using concentration and dosage of alloxan were respectively 1% and 200mg/kg~body weight. After 48 hours of given alloxan, not to fast, the blood glucose of ICR mice was assayed. As long as the blood glucose was large for or equal to 16. 67 mmol/L, the mice were confirmed as diabetic mice. The control group was given only NaCl intraperitoneally at similar dosage. The diabetic and control mice were further and randomly divided into D (diabetic), DV (diabetic + sodiummetavanadate), C (control), CV (control + sodium metavanadate) groups. The DV and CV groups drank aqueous solutions (NaCl 80mmol/L) containing sodium metavanadate (0.2 mg/ml). The D and C groups drank water-containing NaCl 80mmol/L only. All mice drank water freely and the study lasted 5 weeks.At every weekend of the 5 weeks, a regular number of mice were chosen to be assayed the liver glucokinase, muscle hexokinase, blood glucose and insulin.The results showed that the activities of the liver glucokinase and muscle hexokinase were very low in diabetic mice, only about 5% and 8% of the control's levels respectively. After given sodium metavanadate the activities of two enzymes were obviously changed (P<0. 01) . At the 1st weekend the activity levels of the two enzymes had improved to about 61%and 68% of the control's. During the following 2nd to 5th week , the results kept stable0 Oraladministration of sodium metavanadate also had an effect of anti-hyperglycemia in diabetic ICR mice. The effect was independent of insulin but concerned with the activities of the liver glucokinase and muscle hexokinase closely.The conclusion is that, oral administration of sodium metavanadate can reverse the impaired glucose phosphorylation in diabetic ICR mice, which maybe a mechanism of anti-hyperglycemia of oral sodium metavanadate.