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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...

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Bibliographic Details
Published in:The Journal of surgical research 2013-01, Vol.179 (1), p.e83-e90
Main Authors: Xu, Hongzhi, MD, PhD, Yu, Yong-Ming, MD, PhD, Ma, Harry, MD, PhD, Carter, Edward A., PhD, Fagan, Shawn, MD, Tompkins, Ronald G., MD, ScD, Fischman, Alan J., MD, PhD
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Language:English
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Summary: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. Materials and 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 O2 and glucose utilization. Each animal also received a primed constant infusion of [6,6-2 H2 ] 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 O2 consumption and18 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.
ISSN:0022-4804
1095-8673
DOI:10.1016/j.jss.2012.02.037