Study On Hypoglycemic Effect Of Oat Beta-glucan In Mice With Diet-induced Impaired Glucose Regulation

Impaired glucose regulation is an intermediate state between normal and type IIdiabetes, i.e. pre-diabetes. And pre-diabetes symptoms include two states: impairedfasting blood glucose and impaired glucose tolerance. The two states can occurseparately and simultaneously. It is called joint abnormal glucose tolerance when theyoccur simultaneously. The purpose of this article is to establish an animal model whichcan be used in the evaluation of functional food in blood glucose regulation, i.e. ananimal model with diet-induced impaired glucose regulation. And this animal modelwas applied to evaluate the intervention effect of oat beta-glucan on mice withdiet-induced impaired glucose regulation. Then the possible mechanism inhyperglycemic process of oat beta-glucan was discussed from aspects of insulintolerance, insulin resistance, hepatic glucosekinase activity, hepatic glycogen and livertissue morphology.High-fructose and high-fat diet combined with10%(w/v) fructose drinking waterwas applied to establish an animal model with diet-induced impaired glucose regulationsuccessfully. After six weeks, mice of the model control group presented obviousdifference compared with normal control group; After diet induced for eight weeks, thefasting blood glucose level and glucose level after glucose load for two hours of mice inmodel control group was6.1±1.2mmol/L and10.0±2.0mmol/L respectively. Moreover,impaired fasting blood glucose and impaired glucose tolerance, i.e. joint abnormalglucose tolerance, was also presented, which has obvious difference compared withmice of normal control group; After ten weeks, mice of model control group stillremained stable state of impaired fasting blood glucose and impaired glucose tolerance,which has obvious difference compared with mice of normal control group.Mice with impaired glucose regulation still received high-fructose and high-fat dietand10%(w/v) fructose drinking water as the only source of water, at the same time,they were received a gavage of high dose, medium dose and low dose of oat beta-glucan(400,200,100mg/kg b.w.) aqueous solutions to evaluate the function of oat beta-glucanin regulating blood glucose. The intervention on mice with impaired glucose regulationof high-dose oat beta-glucan is the most obvious: after intervention for six weeks, thestate of fasting blood glucose of mice in high-dose control group and medium-dosecontrol group was improved, which presented15.6%and16.7%decrease of blood glucose level compared with model control group respectively; After nine weeks, thefasting blood glucose level and glucose level after glucose load for two hours of mice inhigh-dose control group decreased21.6%and15.9%respectively, the state of impairedglucose tolerance was improved, while there was no significant improvement of mice inmedium-dose and low-dose control groups.As it was presented in the insulin tolerance test, the blood glucose level both at70min and90min of mice in high-dose control group were lower than mice in modelcontrol group, and the blood glucose level at90min was75.3%of the fasting bloodglucose level. So the insulin sensitivity of mice in high-dose control group wasimproved, while there was no obvious intervention effect showing in medium-dose andlow-dose control groups; Mice in high-dose and medium-dose control groups exhibited30.3%and27.3%decrease in insulin resistance index, and30.7%and25.4%increase inhepatic glucosekinase activity compared with mice in model control group respectively.Moreover, mice in high-dose control group presented18.8%increase in hepaticglycogen content compared with mice in model control group, while there was noobvious effect presented in low-dose control group. During the trial period, oatbeta-glucan could inhibit fat deposition in the liver tissue of model mice effectively,which presented a dose-effect relationship. That is the effect of high-dose oatbeta-glucan was better than medium-dose and low-dose beta-glucan.