Capaldo B, Cianciaruso B, Napoli R, Andreucci V, Kopple J D, Saccà L
Department of Internal Medicine, University of Naples, Italy.
J Clin Endocrinol Metab. 1990 Jan;70(1):127-33. doi: 10.1210/jcem-70-1-127.
To evaluate the contribution of the splanchnic area to the carbohydrate abnormalities associated with chronic uremia, the splanchnic exchange of glucose and gluconeogenic substrates was quantitated basally and after an iv glucose load in nine uremic patients with impaired glucose tolerance and seven control subjects. In the basal state, blood glucose and splanchnic glucose production were similar in the two groups. During glucose infusion (33 mumol/kg.min for 90 min), blood glucose reached significantly higher levels in the uremic patients than in controls (P less than 0.02). Plasma insulin increased slightly more in uremic patients than in controls (P less than 0.05 at 15 min). Both basal and postglucose glucagon levels were 2- to 3-fold higher in uremic patients than in normal subjects (P less than 0.05-0.02). In both groups, splanchnic glucose balance switched from net output in the basal state (-9.4 +/- 0.5 and -8.0 +/- 1.1 mumol/kg.min in normals and uremics, respectively) to net uptake with glucose infusion. However, this response was less marked in the uremic patients than in normal subjects (P less than 0.05-0.02 at 30 and 90 min). The cumulative net splanchnic glucose balance over the 90-min study period was 538 +/- 55 mumol/kg in normal subjects and 279 +/- 89 in uremic subjects (P less than 0.05). A net splanchnic lactate uptake was present in the basal state in normal (4.2 +/- 0.5 mumol/kg.min) and uremic subjects (3.4 +/- 0.5). During glucose infusion, in normal subjects splanchnic lactate exchange switched to a net output (-4.0 +/- 1.6 mumol/kg.min), whereas in the uremic group it remained as a net uptake (1.1 +/- 0.7) throughout the study period. Splanchnic gluconeogenic amino acid uptake was similar in the two groups in the basal state (1.8 +/- 0.1 mumol/kg.min and 2.2 +/- 0.2 in normal and uremic subjects, respectively). Glucose infusion caused a marked fall in amino acid uptake by liver in normal subjects, whereas no change was observed in the uremic group (0.9 +/- 0.3 and 1.9 +/- 0.2 mumol/kg.min, respectively). Splanchnic glycerol uptake was not different in the two groups in the basal state (0.75 +/- 0.2 and 1.1 +/- 0.2 mumol/kg.min) and decreased to a similar extent during glucose infusion. We conclude the following. 1) In uremic patients with glucose intolerance but normal fasting glycemia, the splanchnic metabolism of glucose and gluconeogenic substrates is normal in the postabsorptive state.(ABSTRACT TRUNCATED AT 400 WORDS)
为评估内脏区域对慢性尿毒症相关碳水化合物异常的影响,对9例糖耐量受损的尿毒症患者和7名对照者在基础状态及静脉输注葡萄糖负荷后,对葡萄糖和糖异生底物的内脏交换进行了定量分析。在基础状态下,两组的血糖和内脏葡萄糖生成相似。在葡萄糖输注期间(33 μmol/kg·min,持续90分钟),尿毒症患者的血糖水平显著高于对照组(P<0.02)。尿毒症患者血浆胰岛素的升高幅度略大于对照组(15分钟时P<0.05)。尿毒症患者基础和葡萄糖负荷后的胰高血糖素水平均比正常受试者高2至3倍(P<0.05 - 0.02)。在两组中,内脏葡萄糖平衡从基础状态的净输出(正常人和尿毒症患者分别为-9.4±0.5和-8.0±1.1 μmol/kg·min)转变为葡萄糖输注时的净摄取。然而,尿毒症患者的这种反应不如正常受试者明显(30和90分钟时P<0.05 - 0.02)。在90分钟的研究期间,正常受试者的累积内脏葡萄糖净平衡为538±55 μmol/kg,尿毒症受试者为279±89 μmol/kg(P<0.05)。正常(4.2±0.5 μmol/kg·min)和尿毒症受试者(3.4±0.5)在基础状态下均存在内脏乳酸净摄取。在葡萄糖输注期间,正常受试者的内脏乳酸交换转变为净输出(-4.0±1.6 μmol/kg·min),而在尿毒症组中,整个研究期间仍为净摄取(1.1±0.7)。两组在基础状态下内脏糖异生氨基酸摄取相似(正常人和尿毒症受试者分别为1.8±0.1和2.2±0.2 μmol/kg·min)。葡萄糖输注导致正常受试者肝脏对氨基酸的摄取显著下降,而尿毒症组未观察到变化(分别为0.9±0.3和1.9±0.2 μmol/kg·min)。两组在基础状态下内脏甘油摄取无差异(0.75±0.2和1.1±0.2 μmol/kg·min),在葡萄糖输注期间下降程度相似。我们得出以下结论。1)在糖耐量受损但空腹血糖正常的尿毒症患者中,吸收后状态下葡萄糖和糖异生底物的内脏代谢正常。(摘要截短至400字)