Objective　To deter mice the role of glucose in the control of insulin secretion and the possible mechanisms with which glucose fails to exert its effects on adenosine triphosphate-sensitive K＋ channels. Methods NMRI mice islets were used to investigate the amount of insulin secretion and the changes of energy state in islets when the activity of adenosine triphosphate-sensitive K＋channels was eliminated by diazoxide. Isolated islets were cutured in PRMI1640 medium for 18 hours, and were divided into 6 batches randomly, with 10 islets per batch （n＝20）. These were placed in 1.0 ml Krebs medium containing 250 μ mol/L diazoxide, 30 mmol/LK＋and variou glucose concentrations, respectively, and incubated in 37℃ water for 60 minutes. A portion of the supernatant was withdrawn at the end of the incubation for insulin assay, the islets were treated with trichloracetic acid and diethyl ether for the measurements of ATP, ADP, GTP, and UTP. Results　Under our experimental conditions, insulin secretion increased from 3.79± 0.21 to 10.32±0.37 ng/islet （P＜0.010） with the rise of glucose concentrations from 0 to 20 mmol/L.At the same time, the ATP level increased from 7.88±0.20 to 19.62±0.48 pmol/islet （P＜0.01）, and the ADP level decreased gradually from 3.00±0.08 to 1.53±0.08 pmol/islet （P＜0.01）. The ATP/ADP ratio in islets correlated with the rate of insulin secretion （r＝0.9558, P＜0.001）. The GTP and UTP levels also increased from 1.60±0.06 to 4.34±0.09 pmol/islet （P＜0.01） and 0.41±0.02 to 3.31±0.08 pmol/islet （P＜0.01） respectively in the whole range of glucose concentrations. Conclusions　Our findings suggest that glucose can control insulin secretion independently from its actions on adenosine triphosphate-sensitive K＋ channels. In addition, ATP/ADP ratio is an important factor in this mechanism, and GTP and UTP are involved in the control of insulin secretion.