Adolph M, Eckart A, Eckart J
Klinik für Anästhesiologie und operative Intensivmedizin, Krankenhauszweckverband Augsburg.
Anaesthesist. 1995 Nov;44(11):770-81. doi: 10.1007/s001010050212.
Parenteral nutrition required following surgery or injury should not only meet post-aggression caloric requirements but also match the specific metabolic needs so as not to worsen the metabolic disruptions already present in this situation. The primary objective of parenteral nutrition is body protein maintenance or restoration by reduction of protein catabolism or promotion of protein synthesis or both. Whether all parenteral energy donors, ie., glucose, fructose, other polyols, and lipid emulsions, are equally capable of achieving this objective continues to be a controversial issue. The objective of the present study was to answer the following questions: (1) Do glucose and fructose differ in their effects on the metabolic changes seen following surgery or injury, the changes in glucose metabolism in particular? (2) Can the observation of poorer glucose utilization in the presence of lipids be confirmed in ICU patients?
PATIENTS, MATERIALS AND METHODS: A prospective, randomized clinical trial has been conducted in 20 aseptic surgical ICU patients to generate an objective database along these lines by performing a detailed analysis of the metabolic responses to different parenteral nutrition protocols. The effects of a glucose solution+lipid emulsion regimen vs fructose solution+lipid emulsion regimen on a number of carbohydrate and lipid metabolism variables were evaluated for an isocaloric (carbohydrates: 0.25 g/kg body weight/h; lipids: 0.166g/kg body weight/h) and isonitrogenous (amino acids: 0.0625 g/kg body weight/h) total nutrient supply over a 10-h study period.
A significantly smaller rise in blood glucose concentrations (increase from baseline: glucose+lipids P<0.001 vs fructose+lipids n.s.) suggested that fructose had a small effect, if any at all, on glucose metabolism. Serum insulin activity showed significant differences as a function of carbohydrate regimen, i.e. infusion of fructose instead of glucose produced a less pronounced increase in insulin activity (increase from baseline: glucose+lipids P<0.001 vs fructose+lipids P<0.01). Impairment of glucose utilization by concomitant administration of lipids was observed neither in patients who first received glucose nor in those who first received fructose.
As demonstrated, parenteral fructose, unlike parenteral glucose, has a significantly less adverse impact than glucose on the glucose balance, which is disrupted initially in the post-aggression state. In addition, the less pronounced increase in insulin activity during fructose infusion than during glucose infusion can be assumed to facilitate mobilization of endogenous lipid stores and lipid oxidation. Earlier workers pointed out that any rise in free fatty acid and ketone body concentrations in the serum produces inhibition of muscular glucose uptake and oxidation, and of glycolysis. These findings were recorded in a rat model and could not be confirmed in our post-aggression state patients receiving lipid doses commensurate with the usual clinical infusion rates. The serious complications that can result from hereditary fructose intolerance are completely avoidable if a careful patient history is taken before the first parenteral use of fructose. If the patient or family members and close friends, are simply asked whether he/she can tolerate fruit and sweet dishes, hereditary fructose intolerance can be ruled out beyond all reasonable doubt. Only in the extremely rare situations in which it is not possible to question either the patient or any significant other, a test dose will have to be administered to exclude fructose intolerance. The benefits of fructose-specific metabolic effects reported in the literature and corroborated by the results of out own study suggest that fructose is an important nutrient that contributes to metabolic stabilization, especially in the post-aggression phase and in septic patients. Hyperglycaemic states are largely prevented and fewer patients require ex
手术后或受伤后所需的肠外营养不仅应满足应激后的热量需求,还应匹配特定的代谢需求,以免加重这种情况下已存在的代谢紊乱。肠外营养的主要目标是通过减少蛋白质分解代谢或促进蛋白质合成或两者兼而有之来维持或恢复机体蛋白质。所有肠外能量供体,即葡萄糖、果糖、其他多元醇和脂质乳剂,是否同样能够实现这一目标仍然是一个有争议的问题。本研究的目的是回答以下问题:(1)葡萄糖和果糖对手术后或受伤后出现的代谢变化,特别是葡萄糖代谢变化的影响是否不同?(2)在重症监护病房(ICU)患者中能否证实存在脂质时葡萄糖利用较差的观察结果?
患者、材料和方法:对20例无菌手术ICU患者进行了一项前瞻性随机临床试验,通过对不同肠外营养方案的代谢反应进行详细分析,生成沿此方向的客观数据库。在10小时的研究期间,评估了葡萄糖溶液+脂质乳剂方案与果糖溶液+脂质乳剂方案对一些碳水化合物和脂质代谢变量的影响,总营养供应为等热量(碳水化合物:0.25 g/kg体重/小时;脂质:0.166 g/kg体重/小时)和等氮(氨基酸:0.0625 g/kg体重/小时)。
血糖浓度升高明显较小(与基线相比的增加:葡萄糖+脂质P<0.001,果糖+脂质无显著差异),表明果糖对葡萄糖代谢的影响很小(如果有影响的话)。血清胰岛素活性显示出作为碳水化合物方案的函数的显著差异,即输注果糖而非葡萄糖导致胰岛素活性增加不太明显(与基线相比的增加:葡萄糖+脂质P<0.001,果糖+脂质P<0.01)。在首先接受葡萄糖的患者和首先接受果糖的患者中均未观察到脂质同时给药对葡萄糖利用的损害。
如所示,与肠外葡萄糖不同,肠外果糖对葡萄糖平衡的不利影响明显小于葡萄糖,而葡萄糖平衡在应激后状态下最初会受到破坏。此外,果糖输注期间胰岛素活性的增加不如葡萄糖输注期间明显,可以认为这有助于内源性脂质储存的动员和脂质氧化。早期研究人员指出,血清中游离脂肪酸和酮体浓度的任何升高都会抑制肌肉对葡萄糖的摄取和氧化以及糖酵解。这些发现是在大鼠模型中记录的,在我们接受与通常临床输注速率相当的脂质剂量的应激后状态患者中无法得到证实。如果在首次肠外使用果糖之前仔细询问患者病史,遗传性果糖不耐受可能导致的严重并发症是完全可以避免的。如果只是简单询问患者或其家庭成员及亲密朋友他/她是否能耐受水果和甜食,遗传性果糖不耐受几乎可以毫无疑问地被排除。只有在极少数情况下,无法询问患者或任何重要他人时,才必须给予试验剂量以排除果糖不耐受。文献中报道并得到我们自己研究结果证实的果糖特异性代谢效应的益处表明,果糖是一种重要的营养素,有助于代谢稳定,特别是在应激后阶段和脓毒症患者中。高血糖状态在很大程度上得到预防,需要额外……(原文此处不完整)