title: Glucose metabolism during the early "flow phase" after burn injury.
abstract: BACKGROUND
  Burn injury (BI) is associated with insulin resistance (IR) and hyperglycemia which complicate clinical management. We investigated the impact of BI on glucose metabolism in a rabbit model of BI using a combination of positron emission tomography (PET) and stable isotope studies under euglycemic insulin clamp (EIC) conditions.
  
  
  METHODS
  Twelve male rabbits were subjected to either full-thickness BI (B) or sham burn. An EIC condition was established by constant infusion of insulin, concomitantly with a variable rate of dextrose infusion 3 d after treatment. PET imaging of the hind limbs was conducted to determine the rates of peripheral O(2) and glucose utilization. Each animal also received a primed constant infusion of [6,6-(2)H(2)] glucose to determine endogenous glucose production.
  
  
  RESULTS
  The fasting blood glucose in the burned rabbits was higher than that in the sham group. Under EIC conditions, the sham burn group required more exogenous dextrose than the B group to maintain blood glucose at physiological levels (22.2 ± 2.6 versus 13.3 ± 2.9 mg/min, P < 0.05), indicating a state of IR. PET imaging demonstrated that the rates of O(2) consumption and (18)F 2-fluoro-2-deoxy-D-glucose utilization by skeletal muscle remained at similar levels in both groups. Hepatic gluconeogenesis determined by the stable isotope tracer study was found significantly increased in the B group.
  
  
  CONCLUSIONS
  These findings demonstrated that hyperglycemia and IR develop during the early "flow phase" after BI. Unsuppressed hepatic gluconeogenesis, but not peripheral skeletal muscular utilization of glucose, contributes to hyperglycemia at this stage.
authors.affiliation: Department of Surgery, Massachusetts General Hospital, Harvard Medical School and Shriners Hospitals for Children, Boston, Massachusetts, USA. hongzhi2008@gmail.com
authors.forename: Hongzhi
authors.initials: H
authors.lastname: Xu
authors.forename: Yong-Ming
authors.initials: YM
authors.lastname: Yu
authors.forename: Harry
authors.initials: H
authors.lastname: Ma
authors.forename: Edward A
authors.initials: EA
authors.lastname: Carter
authors.forename: Shawn
authors.initials: S
authors.lastname: Fagan
authors.forename: Ronald G
authors.initials: RG
authors.lastname: Tompkins
authors.forename: Alan J
authors.initials: AJ
authors.lastname: Fischman
mesh_terms: D000818:Animals; D002056:Burns / Q000378:metabolism* / Q000503:physiopathology; D005943:Gluconeogenesis / Q000502:physiology; D005947:Glucose / Q000378:metabolism*; D006943:Hyperglycemia / Q000503:physiopathology*; D007333:Insulin Resistance / Q000502:physiology*; D008099:Liver / Q000000981:diagnostic imaging / Q000378:metabolism; D008297:Male; D023421:Models, Animal; D018482:Muscle, Skeletal / Q000000981:diagnostic imaging / Q000378:metabolism; D049268:Positron-Emission Tomography; D011817:Rabbits
chemical_list: D005947:Glucose