REGULATION OF KETONE-BODY FLUX IN SEPTIC PATIENTS

REGULATION OF KETONE-BODY FLUX IN SEPTIC PATIENTS
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DOI:
10.1152/ajpendo.1989.257.5.e665
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发表时间:
1989-11-01
影响因子:
--
通讯作者:
BOULETREAU, P
BOULETREAU, P
中科院分区:
其他
文献类型:
--
作者:
BEYLOT, M;GUIRAUD, M;BOULETREAU, P

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为了评估脓毒症对人体酮体(KB)动力学的影响,我们在正常和脓毒症受试者中测量了游离脂肪酸(FFA)水平升高之前(初始状态)和期间(静脉输注甘油三酯乳剂)的KB出现率(Ra)。我们研究了吸收后状态的正常受试者和脓毒症患者接受低热量静脉输注葡萄糖和氨基酸或12小时后中断。当接受葡萄糖和氨基酸输注时,脓毒症患者的葡萄糖和胰岛素水平高于正常受试者,尽管FFA浓度较低(255 . ±. 44对480。+-。51 μ mol/l,P < 0.05)相当的初始KB Ra(2.50 ± 0.05)。0.10与2.48 .+-. 0.30μ mol·cntdot. kg-1. min ~(-1)。甘油三酯输注使FFA增加至相当的值(败血症780 ± 0.01)。130,正常730。45 μ mol/l),但在脓毒症患者中KB Ra仅上升至3.7 ±。1.1而不是7.7 +-。1.1μ mol·cntdot. kg-1. min ~(-1)与正常对照组比较差异有显著性(P < 0.05)。输注生长抑素可降低脓毒症患者的高胰岛素血症,但不能恢复正常的生酮。在营养输注中断后,脓毒症患者FFA水平正常,只有轻度高血糖和高胰岛素血症。他们最初的KB Ra没有修改。然而,它们对KB Ra的响应(增加到6.27 ±. 2.0μ mol·cntdot. kg-1. min-1)至升高的FFa水平(842 . 170 μ mol/l)与正常受试者的反应相当。总之,尽管接受低热量肠外营养的脓毒症患者生酮功能低下,但在短时间热量剥夺后,他们能够恢复正常的生酮能力。葡萄糖和/或胰岛素似乎在肝生酮的这种调节中起主要作用。
To assess the effect of sepsis on ketone body (KB) kinetics in humans, we measured in normal and septic subjects KB appearance rate (Ra) before (initial state) and during a rise of free fatty acids (FFA) level (intravenous infusion of a triglycerides emulsion). We studied normal subjects in postabsorptive state and septic patients when receiving an hypocaloric intravenous infusion of glucose and amino acids or 12 h after its interruption. When receiving glucose and amino acids infusion, septic patients had higher glucose and insulin levels than normal subjects, and despite lower FFA concentrations (255 .+-. 44 vs. 480 .+-. 51 .mu.mol/1, P < 0.05) comparable initial KB Ra (2.50 .+-. 0.10 vs. 2.48 .+-. 0.30 .mu.mol .cntdot. kg-1 .cntdot. min-1). Triglyceride infusion increased FFA to comparable values (septic 780 .+-. 130, normal 730 .+-. 45 .mu.mol/l), but KB Ra rose in septic patients only to 3.7 .+-. 1.1 instead of 7.7 .+-. 1.1 .mu.mol .cntdot. kg-1 .cntdot. min-1 as in normal subjects (P < 0.05). Somatostatin infusion decreased the hyperinsulinemia of septic patients but did not restore a normal ketogenesis. After interruption of nutriment infusion, septic patients had normal FFA levels and only mild hyperglycemia and hyperinsulinemia. Their initial KB Ra was not modified. However, their response of KB Ra (increase to 6.27 .+-. 2.0 .mu.mol .cntdot. kg-1 .cntdot. min-1) to raised FFa levels (842 .+-. 170 .mu.mol/l) was comparable to the response of normal subjects. In conclusion, although septic patients receiving an hypocaloric parenteral nutrition had a depressed ketogenesis they were able to restore a normal ketogenic capacity after a short-time caloric deprivation. Glucose and/or insulin appears to have a major role in this modulation of hepatic ketogenesis.