AIM:In human sepsis,a prominent component of thehypermetabolite is impaired glucose tolerance (IGT) andhyperglycemia.Elevations in plasma glucose concentrationimpair immune function by altering oltokine production frommacrophages.We assessed the role of glucose in theregulation of circulating levels of insulin,glucagon,cortisol,IL-6 and TNF-α in human sepsis with normal or impairedglucose tolerance.METHODS:According to the results of intravenousglucose tolerance test,forty patients were classified intotwo groups:control group (n=20) and IGT group (n=20).Plasma glucose levels were acutely raised in two groupsand maintained at 15 mmol/L for 3 hours.Plasma insulin,glucagon and cortisol levels were measured byradioimmunoassay,the levels of TNF-α and IL-6 weredetected by ELISA.RESULTS:In IGT group,the fasting concentrations ofplasma glucose,insulin,glucagon,cortisol,IL-6 and TNF-α levels were significantly higher than those in control group(P<0.05).During clamp,the control group had a higheraverage amount of dextrose infusion than the IGT group(P<0.01).In control group,plasma insulin levels rose froma basal value to a peak at an hour (P<0.05) and maintainedat high levels.Plasma glucagon levels descended from abasal value to the lowest level within an hour (P<0.01)and low levels were maintained throughout the clamp.InIGT group,plasma insulin was more significantly elevated(P<0.01),and plasma glucagon levels were not significantlydeclined.Plasma cortisol levels were not significantly changedin two groups.In control group,plasma IL-6 and TNF-α levelsrose (P<0.01) within 2 hours of the clamp and returned tobasal values at 3 hours.In IGT group,increased levels ofplasma cytokine lasted longer than in control group (3 hoursvs.2 hours,P<0.05),and the cytokine peaks of IGT groupwere higher (P<0.05) than those of control group.CONCLUSION: Acute hyperglycemia pricks up hyperinsulinemia and increases circulating cytokine concentrations and these effects are more pronounced in sepsis with IGT. This suggests a potential modulation of immunoinflammatory responses in human sepsis by hyperglycemia. AIM: In human sepsis, a prominent component of the hypermetabolite is impaired glucose tolerance (IGT) and hyperglycemia. Elevations in plasma glucose concentration of immune function by altering oltokine production from macrophages. We assessed the role of glucose in thereulation of circulating levels of insulin, glucagon, cortisol , IL-6 and TNF-α in human sepsis with normal or impaired glucose tolerance. METHODS: According to the results of intravenous glucose tolerance test, forty patients were classified intotwo groups: control group (n = 20) and IGT group Plasma levels were acutely raised in two groups and maintained at 15 mmol / L for 3 hours. Plasma matrices, glucagon and cortisol levels were measured by radioimmunoassay, the levels of TNF-α and IL-6 weredetected by ELISA.RESULTS: In IGT group , the fasting concentrations of plasma glucose, insulin, glucagon, cortisol, IL-6 and TNF-α levels were significantly higher than those in control groups (P <0.05) In control group, plasma insulin levels rose froma basal value to a peak at an hour (P <0.05) and maintainedat high levels. Plasma placagon levels descended from abasal value to plasma level was significantly increased (P <0.01), and plasma levels of plasma glucagon were significantly increased (P <0.01) two groups.In control group, plasma IL-6 and TNF-α levelsrose (P <0.01) within 2 hours of the clamp and returned tobasal values ​​at 3 hours. IGT group, increased levels of plasma cytokine lasted longer than in control group ( 3 hours vs. 2 hours, P <0.05), and the cytokine peaks of IGT groupwere higher (P <0.05) than those of control group. CONCLUSION: Acute hyperglycemia pricks up hyperinsulinemia and increases circulating cytokine concentrations and these effects are more pronounced in se psis with IGT. This suggests a potential modulation of immunoinflammatory responses in human sepsis by hyperglycemia.