Intensive insulin therapy improves insulin sensitivity and mitochondrial function in severely burned children

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Reference Type:
Journal Article
Accession No.:
Critical Care Medicine
Year, Volume, Issue, Page(s):
2010, vol. 38, issue 6, pp 1475-1483
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Study examined the effects of an intensive insulin therapy protocol in an acute pediatric burn unit and the mechanisms underlying its benefits. Twenty children, 4 to 18 years old, with total body surface area burned greater than 40 percent and who arrived within 1 week after injury were included in the data analysis. Patients were randomized to one of two groups: (1) intensive insulin therapy maintained blood glucose levels between 80 and 110 milligrams per deciliter (mg/dL) or (2) conventional insulin therapy maintained blood glucose <215 mg/dL. Metabolic studies were performed at 7 days postburn (pretreatment) and at 21 days postburn (posttreatment). Resting energy expenditure, whole body and liver insulin sensitivity, and skeletal muscle mitochondrial function were the primary outcomes examined. Results indicated that resting energy expenditure significantly increased after treatment in conventional insulin therapy group as compared with a decline in intensive insulin therapy. Glucose infusion rate was identical between groups before treatment. Intensive insulin therapy displayed a significantly higher glucose clamp infusion rate posttreatment. Suppression of hepatic glucose release was significantly greater in the intensive insulin therapy group after treatment compared with conventional insulin therapy. States 3 and 4 mitochondrial oxidation of palmitate significantly improved in intensive insulin therapy, whereas conventional insulin therapy remained at the same level of activity. The findings suggest that controlling blood glucose levels at <120 mg/dL using an intensive insulin therapy protocol improves insulin sensitivity and mitochondrial oxidative capacity while decreasing resting energy expenditure in severely burned children.
Fram RY, Cree MG, Wolfe RR, Mlcak RP, Qian T, Chinkes DL, Herndon DN
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