Sacca L, Hendler R, Sherwin R S
J Clin Endocrinol Metab. 1978 Nov;47(5):1160-3. doi: 10.1210/jcem-47-5-1160.
To evaluate the influence of hyperglycemia on hepatic glucose output in the absence of a rise in insulin, glucose was infused for 2 hours into six juvenile-onset diabetics receiving a constant infusion of insulin at a rate of 0.05-0.15 microM kg-1min-1. Prior to the infusion of glucose, insulin administration resulted in stable levels of plasma glucose (76 +/- 8 mg/dl) and glucose output (1.9 +/- 0.1 mg kg-1min-1). The addition of glucose produced a 2-3 fold rise in plasma glucose and a prompt fall in glucose output to 0.2-0.4 mg kg-1min-1, despite the unchanged rate of insulin infusion and the absence of a reduction in plasma glucagon or catecholamines. A similar decline in glucose output was observed when exogenous glucagon (1 ng kg-1-min-1) was added to the glucose infusion. We conclude that in the presence of basal insulin levels hyperglycemia inhibits glucose output independent of a rise in insulin or a fall in anti-insulin hormones.
为了评估在胰岛素不升高的情况下高血糖对肝脏葡萄糖输出的影响,以0.05 - 0.15微摩尔/千克·分钟的速率持续输注胰岛素,同时向6名青少年发病型糖尿病患者输注葡萄糖2小时。在输注葡萄糖之前,胰岛素给药导致血浆葡萄糖(76±8毫克/分升)和葡萄糖输出(1.9±0.1毫克/千克·分钟)水平稳定。尽管胰岛素输注速率不变且血浆胰高血糖素或儿茶酚胺没有降低,但添加葡萄糖使血浆葡萄糖升高2 - 3倍,并使葡萄糖输出迅速降至0.2 - 0.4毫克/千克·分钟。当向葡萄糖输注中添加外源性胰高血糖素(1纳克/千克·分钟)时,观察到葡萄糖输出有类似下降。我们得出结论,在基础胰岛素水平存在时,高血糖抑制葡萄糖输出,这与胰岛素升高或抗胰岛素激素降低无关。