INFLUENCE OF MATURITY-ONSET DIABETES ON SPLANCHNIC GLUCOSE BALANCE AFTER ORAL GLUCOSE INGESTION
INFLUENCE OF MATURITY-ONSET DIABETES ON SPLANCHNIC GLUCOSE BALANCE AFTER ORAL GLUCOSE INGESTION
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DOI：
10.2337/diab.27.2.121
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发表时间：
1978-01-01
期刊：
影响因子：
7.7
通讯作者：
HENDLER, R
中科院分区：
文献类型：
--
作者：
FELIG, P;WAHREN, J;HENDLER, R
为了确定改变的内脏葡萄糖平衡在多大程度上促进了糖尿病患者餐后高血糖，在7名成熟型糖尿病患者和10名健康对照者的基础状态下，在口服100 g葡萄糖3小时后，测定了内脏葡萄糖交换。在基础禁食状态下，糖尿病患者的动脉葡萄糖水平(153 .+-。24 mg/100 ml)比对照组高75 ~ 80 mg/100 ml，而两组内脏葡萄糖输出量相似（132 ~ 145 mg/min）。葡萄糖摄入后，糖尿病患者的动脉葡萄糖浓度上升到峰值水平(295。35 mg/100 ml)，比对照组高55%，葡萄糖后3小时仍比基础水平高100-125 mg/100 ml，比对照水平高150-200 mg/100 ml。在葡萄糖喂养后15-30分钟，糖尿病患者的内脏葡萄糖输出量迅速上升至基础水平的4倍，并在整个3小时内保持比基础水平高60%或更多。相比之下，在对照组中，在类似的早期升高之后，内脏葡萄糖输出在90分钟后恢复到基础水平。结果，糖尿病患者在3小时内的总内脏葡萄糖输出量(53。4 g)比对照组高33%。糖尿病患者内脏葡萄糖输出高于基础水平的增加(30。5 g)比对照组高100%，可以解释3小时观察到的体液中葡萄糖积累增加的75%。在成熟型糖尿病患者中，净内脏葡萄糖输出在葡萄糖摄入后增加，这表明口服葡萄糖负荷进入体循环的比例比健康对照大。内脏葡萄糖潴留失败是导致成熟型糖尿病餐后高血糖的主要因素。
To determine the extent to which altered splanchnic glucose balance contributes to postprandial hyperglycemia in diabetes, splanchnic glucose exchange was determined in 7 maturity-onset diabetics and 10 healthy control subjects in the basal state and for 3 h following oral ingestion of 100 g of glucose. In the basal fasting state, arterial glucose levels in the diabetics (153 .+-. 24 mg/100 ml) were 75-80 mg/100 ml higher than in controls while splanchnic glucose output was similar in the 2 groups (132-145 mg/min). Following glucose ingestion, arterial glucose concentration in the diabetics rose to peak levels (295 .+-. 35 mg/100 ml) that were 55% higher than in controls and remained 100-125 mg/100 ml above basal levels and 150-200 mg/100 ml above control levels 3 h after glucose. Splanchnic glucose output rose rapidly in the diabetics to values 4 times the basal rate at 15-30 min after glucose feeding and remained 60% or more above basal levels throughout the 3 h period. In contrast, in the controls following a similar early rise, splanchnic glucose output returned to basal levels by 90 min. As a consequence, total splanchnic glucose output over 3 h in the diabetics (53 .+-. 4 g) was 33% greater than in controls. The increment in splanchnic glucose output above basal levels in the diabetics (30 .+-. 5 g) was 100% greater than in controls and could account for 75% of the augmented glucose accumulation in body fluids observed at 3 h. In maturity-onset diabetics net splanchnic glucose output is increased after glucose ingestion, suggesting that a greater proportion of an oral glucose load enters the systemic circulation than in healthy controls. Failure of splanchnic glucose retention is the major factor responsible for postprandial hyperglycemia in maturity-onset diabetes.