Wahren J
Lancet. 1976 Dec 4;2(7997):1213-6. doi: 10.1016/s0140-6736(76)91142-9.
Infusion of somatostatin, an inhibitor of glucagon secretion, in insulin-dependent diabetics resulted in a 75-100% reduction in the blood-glucose rise after oral glucose administration, but did not improve intravenous glucose tolerance. Somatostatin reduced blood-xylose levels by 50-90% after ingestion of this pentose and delayed the peak increment in blood-xylose by 1-2 h. Similar effects on blood-xylose levels and a 30% reduction in splanchnic blood-flow were observed in normal subjects during infusion of somatostatin. Glucagon administration (3 ng per kg per min) or intraduodenal administration of xylose did not reverse somatostatin's effect on xylose tolerance. Somatostatin reduces postprandial hyperglycaemia in diabetes primarily by decreasing and/or delaying carbohydrate absorption rather than enhancing carbohydrate disposal. This effect may be mediated, in part, but a reduction in splanchnic blood-flow. These findings indicate that postprandial hyperglycaemia in diabetes is due primarily to insulin deficiency rather than glucagon excess.
给胰岛素依赖型糖尿病患者输注胰高血糖素分泌抑制剂生长抑素,口服葡萄糖后血糖升高幅度降低了75% - 100%,但静脉葡萄糖耐量并未改善。摄入这种戊糖后,生长抑素使血木糖水平降低了50% - 90%,并使血木糖峰值升高延迟了1 - 2小时。在正常受试者输注生长抑素期间,观察到对血木糖水平有类似影响,且内脏血流量减少了30%。给予胰高血糖素(每分钟每千克3纳克)或十二指肠内给予木糖并不能逆转生长抑素对木糖耐量的影响。生长抑素降低糖尿病患者餐后高血糖主要是通过减少和/或延迟碳水化合物吸收,而非增强碳水化合物代谢。这种作用可能部分是由内脏血流量减少介导的。这些发现表明,糖尿病患者餐后高血糖主要是由于胰岛素缺乏而非胰高血糖素过多。