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Burn-induced insulin resistance is associated with increased morbidity andmortality; however, the impact of burn injury on tissue-specific insulinsensitivity and its molecular mechanisms with consideration of insulin stateremains unknown in rodent models. This study was designed to characterize aburn mouse model with tissue-specific insulin resistance under insulin clampconditions. C57BL6/J mice were subjected to 30% full-thickness burn injury andunderwent the combination of hyperinsulinemic isoglycemicclamp (HIC) andpositron emission tomography (PET). Hepatic glucose production (HGP) andperipheral glucose disappearance rate (Rd) were measured at different timepoints up to 7 days post injury. Burned mice showed a significant fastinghypoglycemia and hypoinsulinemia (P < 0.01) on post-burn day (PBD) 3 and 7along with significantly higher energy expenditure (P < 0.01). HICon PBD 3demonstrated that burn injury induced systemic insulin resistance, resultingfrom a significant decrease in insulin-stimulated Rd (33.0 +/- 10.2 vs 68.3 +/-5.9 mg/kg/min; P < 0.05). In contrast, HGP of burned and sham mice wascomparable both in the basal and clamp period. PET on PBD 3 showed a lowerinsulin-stimulated 18F-labeled 2-fluoro-2-deoxy-D-glucose uptake in thequadriceps of burned mice compared with sham-burned mice. Gastrocnemius muscleharvested from burned mice on PBD 3 showed decreased insulin-stimulatedtyrosine phosphorylation of insulin receptor substrate-1 to 34.7% of that insham-burn mice by immunoblotting analysis (P < 0.05). These findings suggestthat impaired insulin-stimulated Rd in skeletal muscle, not elevated HGP, playsa role in the development of burn-induced insulin resistance in a mouse model.

Impairment of insulin-stimulated glucose utilization is associated with  burn-induced insulin resistance in mouse muscle by  hyperinsulinemic-isoglycemic clamp