Metabolism Unit and Department of Surgery, The University of Texas Medical Branch, Galveston, TX, USA.
Crit Care Med. 2010 Jun;38(6):1475-83. doi: 10.1097/CCM.0b013e3181de8b9e.
To institute intensive insulin therapy protocol in an acute pediatric burn unit and study the mechanisms underlying its benefits.
Prospective, randomized study.
An acute pediatric burn unit in a tertiary teaching hospital.
Children, 4-18 yrs old, with total body surface area burned > or =40% and who arrived within 1 wk after injury were enrolled in the study.
Patients were randomized to one of two groups. Intensive insulin therapy maintained blood glucose levels between 80 and 110 mg/dL. Conventional insulin therapy maintained blood glucose < or =215 mg/dL.
Twenty patients were included in the data analysis consisting of resting energy expenditure, whole body and liver insulin sensitivity, and skeletal muscle mitochondrial function. Studies were performed at 7 days postburn (pretreatment) and at 21 days postburn (posttreatment). Resting energy expenditure significantly increased posttreatment (1476 +/- 124 to 1925 +/- 291 kcal/m(2) x day; p = .02) in conventional insulin therapy as compared with a decline in intensive insulin therapy. Glucose infusion rate was identical between groups before treatment (6.0 +/- 0.8 conventional insulin therapy vs. 6.8 +/- 0.9 mg/kg x min intensive insulin therapy; p = .5). Intensive insulin therapy displayed a significantly higher glucose clamp infusion rate posttreatment (9.1 +/- 1.3 intensive insulin therapy versus 4.8 +/- 0.6 mg/kg x min conventional insulin therapy, p = .005). Suppression of hepatic glucose release was significantly greater in the intensive insulin therapy after treatment compared with conventional insulin therapy (5.0 +/- 0.9 vs. 2.5 +/- 0.6 mg/kg x min; intensive insulin therapy vs. conventional insulin therapy; p = .03). States 3 and 4 mitochondrial oxidation of palmitate significantly improved in intensive insulin therapy (0.9 +/- 0.1 to 1.7 +/- 0.1 microm O(2)/CS/mg protein/min for state 3, p = .004; and 0.7 +/- 0.1 to 1.3 +/- 0.1 microm O(2)/CS/mg protein/min for state 4, p < .002), whereas conventional insulin therapy remained at the same level of activity (0.9 +/- 0.1 to 0.8 +/- 0.1 microm O(2)/CS/mg protein/min for state 3, p = .4; 0.6 +/- 0.03 to 0.7 +/- 0.1 microm O(2)/CS/mg protein/min, p = .6).
Controlling blood glucose levels < or =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.
在小儿烧伤科建立强化胰岛素治疗方案，并研究其益处的机制。
前瞻性、随机研究。
一家三级教学医院的小儿烧伤科。
4-18 岁，全身烧伤面积>或=40%，伤后 1 周内入院的儿童。
患者随机分为两组。强化胰岛素治疗组将血糖维持在 80-110mg/dL 之间。常规胰岛素治疗组将血糖控制在<或=215mg/dL。
20 名患者纳入数据分析，包括静息能量消耗、全身和肝脏胰岛素敏感性以及骨骼肌线粒体功能。研究分别在烧伤后 7 天（预处理）和 21 天（后处理）进行。与强化胰岛素治疗组相比，常规胰岛素治疗组的静息能量消耗在后处理时显著增加（1476 +/- 124 至 1925 +/- 291kcal/m(2)x 天；p=0.02）。在治疗前，两组的葡萄糖输注率相同（常规胰岛素治疗组为 6.0 +/- 0.8mg/kg x min 与强化胰岛素治疗组的 6.8 +/- 0.9mg/kg x min；p=0.5）。强化胰岛素治疗组在后处理时的葡萄糖钳夹输注率明显更高（强化胰岛素治疗组为 9.1 +/- 1.3mg/kg x min，常规胰岛素治疗组为 4.8 +/- 0.6mg/kg x min，p=0.005）。强化胰岛素治疗组治疗后肝葡萄糖释放的抑制作用明显大于常规胰岛素治疗组（强化胰岛素治疗组为 5.0 +/- 0.9mg/kg x min，常规胰岛素治疗组为 2.5 +/- 0.6mg/kg x min；强化胰岛素治疗组 vs. 常规胰岛素治疗组；p=0.03）。棕榈酸的 3 态和 4 态线粒体氧化作用在强化胰岛素治疗组显著改善（3 态从 0.9 +/- 0.1 至 1.7 +/- 0.1 microm O(2)/CS/mg 蛋白/分钟，p=0.004；4 态从 0.7 +/- 0.1 至 1.3 +/- 0.1 microm O(2)/CS/mg 蛋白/分钟，p<0.002），而常规胰岛素治疗组仍保持相同的活性水平（3 态从 0.9 +/- 0.1 至 0.8 +/- 0.1 microm O(2)/CS/mg 蛋白/分钟，p=0.4；4 态从 0.6 +/- 0.03 至 0.7 +/- 0.1 microm O(2)/CS/mg 蛋白/分钟，p=0.6）。
在严重烧伤儿童中使用强化胰岛素治疗方案控制血糖水平<或=120mg/dL 可改善胰岛素敏感性和线粒体氧化能力，同时降低静息能量消耗。
