HEPATIC, GUT, AND RENAL SUBSTRATE FLUX RATES IN PATIENTS WITH HEPATIC CIRRHOSIS
HEPATIC, GUT, AND RENAL SUBSTRATE FLUX RATES IN PATIENTS WITH HEPATIC CIRRHOSIS
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DOI：
10.1172/jci110240
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发表时间：
1981-01-01
影响因子：
15.9
通讯作者：
BODEN, G
中科院分区：
文献类型：
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作者：
OWEN, OE;REICHLE, FA;BODEN, G
对28例重度肝硬化患者（其中25例为酒精性肝硬化）的肝、肾和肠道在维持燃料稳态中的作用进行了研究。测量肝脏、门静脉和肾脏的血流量，并结合肝脏、肠道和肾脏的底物浓度差异，计算游离脂肪酸、酮体、甘油三酯和葡萄糖与选定葡萄糖前体（包括甘油、乳酸盐、丙酮酸盐和氨基酸）的净通量。导管插入术研究的数据与肝组织学、糖原含量和促肝细胞生成酶的活性有关，并与对照组患者的数据进行比较。在禁食过夜和禁食3天后，评估了食物剥夺对肝脏、肠道和肾脏燃料净流量的影响。肝纤维化的肝脏中，促纤维化酶的活性正常，但肝糖原含量减少，可能是广泛的肝纤维化的结果。在糖尿病患者中，在过夜或禁食3天后，平均肾脏葡萄糖对血流没有贡献。经过一夜的快速肝硬化患者的肝葡萄糖生产减少，由于低速率糖原分解。肝细胞生成和生酮增加。这种肝脏代谢模式模拟了正常患者在更晚期饥饿后所见的情况。经过3天的饥饿，肝硬化患者的肝硬化和生酮配置文件进行类似的时间饥饿的正常患者。来自酮体加上葡萄糖的热量当量的总数校正循环乳酸盐和丙酮酸盐添加到血液中，可以由外周组织的终末氧化的黄疸的肝脏是小于正常肝脏的贡献，经过一夜之间和3天的快速。
The roles of the liver, kidney and gut in maintaining fuel homeostasis were studied in 28 patients with severe hepatic cirrhosis, 25 of whom had alcohol-induced cirrhosis. Hepatic, portal and renal blood flow rates were measured and combined with substrate concentration differences across liver, gut and kidney to calculate the net flux of free fatty acids, ketone bodies, triglycerides and glucose with selected glucose precursors, including glycerol, lactate, pyruvate and amino acids. Data from the catheterization studies were related to hepatic histology, glycogen content and activities of gluconeogenic enzymes and compared with data obtained from control patients. The effects of food deprivation on net flux of fuels across the liver, gut and kidney were assessed after overnight and after 3 d [day] of fasting. Activities of gluconeogenic enzymes were normal, but hepatic glycogen content was diminished in cirrhotic livers, probably as a consequence of extensive hepatic fibrosis. In cirrhotic patients, there was no mean renal glucose contribution to the bloodstream after an overnight or after a 3-d fast. After an overnight fast hepatic glucose production in patients with cirrhosis was diminished as a result of low-rate glycogenolysis. Hepatic gluconeogenesis and ketogenesis were increased. This pattern of hepatic metabolism mimics that seen in normal patients after more advanced stages of starvation. After 3 d of starvation, patients with hepatic cirrhosis have hepatic gluconeogenic and ketogenic profiles comparable to those of normal patients undergoing starvation of similar duration. The total number of caloric equivalents derived from ketone bodies plus glucose corrected for recycled lactate and pyruvate added to the bloodstream by the cirrhotic livers that could be terminally oxidized by peripheral tissues was less than the contributions made by the normal livers, after an overnight and after a 3-d fast.