Sherwin R S
Acta Chir Scand Suppl. 1981;507:30-40.
To evaluate the effect ketone bodies on protein metabolism beta-hydroxybutyrate was infused into healthy nonobese and obese subjects and insulin dependent diabetics in the postabsorptive state and into obese subjects after 3 days and 3-10 wks of starvation. In association with blood ketone increments of 1-2 mM, plasma alanine fell by 25-35% in all treatment groups. Furthermore, the hypoalaninemic effect of beta-hydroxybutyrate was equally demonstrable in fasted subjects, in whom alanine was already reduced. In association with repeated 12 hr infusions of beta-hydroxybutyrate in subjects fasted 5-10 wks, urinary nitrogen fell by 30%, returning to baseline after cessation of the infusions and paralleling the changes in plasma alanine. When endogenous ketonemia was produced by isocaloric carbohydrate restriction (less than 25 gm/day), protein ingestion was associated with a 40-50% greater increase in plasma branched chain amino acids as well as a reduced rise in plasma insulin. The enhanced rise in branched chain amino acids was attributable to decreased net utilization since intravenous leucine also produced a 40% greater elevation in plasma leucine after carbohydrate restriction. When nitrogen balance was compared during hypocaloric (400 Kcal) feeding of a pure protein diet and a mixed diet containing 50% protein and 50% carbohydrate, no significant differences were observed. Isocaloric replacement with carbohydrate failed to accentuate nitrogen wasting, despite a marked lowering of blood and urinary ketones. Our findings support the possibility that ketone bodies contribute to the reduction in proteolysis and decrease in muscle alanine release which characterizes prolonged starvation. However, when endogenous hyperketonemia is induced by carbohydrate restriction, plasma insulin declines and the disposal of ingested protein is impaired. Furthermore, the addition of carbohydrate during hypocaloric feeding reduces hyperketonemia, but does not enhance negative nitrogen balance. These observations suggest that dietary carbohydrate and insulin also promote nitrogen retention and that ketogenic, high protein diets do not confer a unique protein sparing advantage.
为评估酮体对蛋白质代谢的影响，将β-羟基丁酸注入处于吸收后状态的健康非肥胖和肥胖受试者、胰岛素依赖型糖尿病患者，以及饥饿3天和3 - 10周后的肥胖受试者体内。在所有治疗组中，随着血酮增加1 - 2 mM，血浆丙氨酸下降了25 - 35%。此外，β-羟基丁酸的低丙氨酸血症效应在禁食受试者中同样明显，这些受试者的丙氨酸水平已经降低。在禁食5 - 10周的受试者中，与重复12小时输注β-羟基丁酸相关，尿氮下降了30%，输注停止后恢复至基线水平，且与血浆丙氨酸的变化平行。当通过等热量碳水化合物限制（每天少于25克）产生内源性酮血症时，蛋白质摄入与血浆支链氨基酸增加40 - 50%以及血浆胰岛素升高幅度降低相关。支链氨基酸升高幅度的增加归因于净利用率降低，因为在碳水化合物限制后，静脉注射亮氨酸也使血浆亮氨酸升高了40%。当比较低热量（400千卡）纯蛋白质饮食和含50%蛋白质与50%碳水化合物的混合饮食喂养期间的氮平衡时，未观察到显著差异。用碳水化合物进行等热量替代未能加剧氮的浪费，尽管血酮和尿酮明显降低。我们的研究结果支持这样一种可能性，即酮体有助于减少蛋白质分解和肌肉丙氨酸释放的减少，这是长期饥饿的特征。然而，当通过碳水化合物限制诱导内源性高酮血症时，血浆胰岛素下降，摄入蛋白质的处理受损。此外，在低热量喂养期间添加碳水化合物可降低高酮血症，但不会增强负氮平衡。这些观察结果表明，膳食碳水化合物和胰岛素也促进氮的保留，而生酮高蛋白饮食并没有独特的蛋白质节省优势。
