AIM To evaluate the impact of JTN on beta cell function in mice with impaired glucose tolerance (IGT).METHODS Two animal models with IGT were chosen to evaluate the effect of JTN on beta cell function.The MSG obese mice were induced with L-sodium glutamate, which have certain features of prediabetes, such as obesity, impaired glucose tolerance, beta cell dysfunction.KKAy mice characterized with impaired glucose tolerance and moderately hyperglycemia.Both of two IGT mouse models were randomly divided into five groups.Five groups of IGT mice (n =10) were fed for45 d either a 50% sucrose diet (control) or a 50% sucrose diet supplemented with JTN 8, 12, 16 g or acarbose 0.3 g per kilogram chow.Oral glucose tolerance test (OGrTT) and insulin tolerance test were performed.Fasting plasma glucose, TG, TCHO and insulin level were measured at the end of the supplementation.Blood pressure and cataracta of eyes in MSG mice were detected.Pancreatic beta call function was quantified using a hyperglycemic clamp.RESULTS Mter 7 weeks of supplementation, JTN flatted blood glucose peak and reduced the AUC during OGTT compared with the control group.HOMA-β index was significantly higher in JTN groups.Dietary supplementation of JTN improved insulin sensitivity in both MSG and KKAy mice.JTN also decreased the fasting plasma glucose and TG.In hyperglycemic clamps, JTN increased glucose infusion rate (GIR) with dose-dependent fashion in MSG and KKAy mice, which indicated the improved beta cell insulin secretory function.At the end of experiment, JTN also reduced the incidence of cataract in MSG mice.CONCLUSION These results suggested that JTN showed beneficial effect on glucose, lipid metabolism and the diabetic complication which were due to the improvement in insulin sensitivity and beta cell function.