Glucose metabolism during the early “flow phase” after burn injury

Abstract

Background Burn injury (BI) is associated with insulin resistance and hyperglycemia which complicate clinical management. We investigated the impact of BI on glucose metabolism in a rabbit model of burn injury using a combination of PET and stable isotope studies under Euglycemic Insulin Clamp (EIC) conditions. Materials/Methods Twelve male rabbits were subjected to either full thickness burn injury (B) or sham burn (SB). Three days after treatment, an EIC condition was established by constant infusion of insulin, concomitantly with a variable rate of dextrose infusion. 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 [6,6,2H2] glucose to determine endogenous glucose production. Results The fasting blood glucose in the burned rabbits was higher than in the sham group. Under EIC conditions, the SB group required more exogenous dextrose than the B group in order to maintain blood glucose at physiological levels (22.2 ± 2.6 vs 13.3 ± 2.9 mg/min, P < 0.05), indicating a state of insulin resistance. PET imaging demonstrated that the rates of O2 consumption and FDG 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 BI group. Conclusions These findings demonstrated that hyperglycemia and insulin resistance 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.

Mammalian target of rapamycin regulates a hyperresponsive state in pulmonary neutrophils late after burn injury

“…To this end, in addition to immune dysfunction, burn patients also experience severe metabolic dysregulation, characterized by elevated basal metabolic rate and a paradoxical comingling of hyperglycemia and hyperinsulinemia. [17][18][19][20][21] Similarly, several animal studies have demonstrated altered metabolism in animal models of burn injury, including insulin resistance and hyperglycemia. [21][22][23] The relationship between metabolism and immunity has been focus of much recent research activity.…”

“…[17][18][19][20][21] Similarly, several animal studies have demonstrated altered metabolism in animal models of burn injury, including insulin resistance and hyperglycemia. [21][22][23] The relationship between metabolism and immunity has been focus of much recent research activity. 24,25 Insulin receptor signaling suppresses TLR expression in human granulocytes, 26 and hyperglycemia perturbs both cytokine secretion and TLR signaling in myeloid cells.…”

Use of 1H-nuclear magnetic resonance to screen a set of biomarkers for monitoring metabolic disturbances in severe burn patients

“…After severe burn, the stress process is followed and represented by the release of a large amount of stress-related hormones and cytokines. This stress process leads to mal-metabolism of carbohydrates via insulin resistance and hyperglycemia [ 28 ]. For a very long time, researchers and clinical practitioners have considered hyperglycemia post severe burn as a type of stress-related phenomena and quite different from diabetes.…”