Felig P, Wahren J, Hendler R
Diabetes. 1975 May;24(5):468-75. doi: 10.2337/diab.24.5.468.
To evaluate the role of splanchnic and peripheral tissues in the disposal of an oral glucose load, splanchnic exchange of glucose, lactate, pyruvate, glycerol and amino acids was determined in ten healthy subjects in the basal state and for three hours following the oral ingestion of 100 gm. of glucose. Following glucose ingestion, splanchnic glucose output rose rapidly, reaching values two to three times the basal rate at fifteen minutes and returning to baseline by ninety minutes. A secondary rise in splanchnic glucose output occurred at 150 minutes and coincided with a secondary increment in arterial glucose. Total splanchnic glucose output over three hours was 40 plus or minus 3 gm., representing a total increase of only 15 plus or minus 3 gm. above basal splanchnic glucose output. The peak rise in blood glucose was directly proportional to the increase in splanchnic glucose output. Arterial concentrations of alanine, lactate and pyruvate rose by 15, 65 and 80 per cent, respectively, following oral glucose. These arterial elevations were preceded by a 75-100 per cent inhibition of splanchnic uptake of alanine and lactate; in the case of pyruvate there was a reversal from a net uptake in the basal state to a significant net splanchnic output after glucose ingestion. Arterial glycerol fell by 50 per cent and was accompanied by a comparable fall in splanchnic uptake. It is concluded that in normal, postabsorptive man, (a) the major portion of a 100 gm. oral glucose load is retained within the splanchnic bed; (b) only 15 per cent of the ingested glucose is available for disposal by peripheral tissues as increased (above-basal) glucose utilization; (c) the height and shape or the oral glucose tolerance curve are largely determined by the rate and pattern of splanchnic glucose escape; (d) glucose-induced hyperlactatemia, hyperpyruvicemia and hyperalaninemia are due at least in part, to altered splanchnic exchange of these substrates.
为评估内脏和外周组织在处理口服葡萄糖负荷中的作用,对10名健康受试者在基础状态下以及口服100克葡萄糖后的三小时内,测定了葡萄糖、乳酸、丙酮酸、甘油和氨基酸的内脏交换情况。口服葡萄糖后,内脏葡萄糖输出迅速增加,在15分钟时达到基础速率的两到三倍,并在90分钟时恢复到基线水平。在内脏葡萄糖输出在150分钟时出现二次升高,同时动脉葡萄糖也出现二次升高。三小时内总的内脏葡萄糖输出为40±3克,比基础内脏葡萄糖输出仅增加了15±3克。血糖的峰值升高与内脏葡萄糖输出的增加成正比。口服葡萄糖后,动脉中丙氨酸、乳酸和丙酮酸的浓度分别升高了15%、65%和80%。这些动脉浓度的升高之前,内脏对丙氨酸和乳酸的摄取受到75%-100%的抑制;就丙酮酸而言,在基础状态下是净摄取,口服葡萄糖后则转变为显著的内脏净输出。动脉甘油下降了50%,同时内脏摄取也有相应下降。结论是,在正常的吸收后状态的人体中,(a)100克口服葡萄糖负荷的大部分保留在内脏床内;(b)只有15%的摄入葡萄糖可通过外周组织作为增加的(高于基础的)葡萄糖利用来处理;(c)口服葡萄糖耐量曲线的高度和形状在很大程度上由内脏葡萄糖逸出的速率和模式决定;(d)葡萄糖诱导的高乳酸血症、高丙酮酸血症和高丙氨酸血症至少部分是由于这些底物的内脏交换改变所致。