Hand M S, Fettman M J, Chandrasena L G, Cleek J L, Mason R A, Phillips R W
Circ Shock. 1983;11(4):287-95.
The role of hyperinsulinemia in the development of hypoglycemia was evaluated in awake Yucatan minipigs. Eight adult minipigs were fitted with jugular, portal, and hepatic vein and carotid artery catheters, and hepatic artery and portal vein flow cuffs for determination of transhepatic kinetics and insulin secretion. Three days later they were infused with E. coli endotoxin at 15 micrograms/kg/hr. Transient hyperinsulinemia was preceded by an elevation of the rate of glucose uptake (Rd) determined from [6-3H] glucose-specific activity. This finding suggested that hyperinsulinemia might be caused by, and then be contributory to, increased Rd. If an increase in glucose uptake was also experienced by pancreatic beta-cells, the existing glycemic state could be overestimated and an inappropriate insulin release elicited.
在清醒的尤卡坦小型猪中评估了高胰岛素血症在低血糖发生中的作用。八只成年小型猪安装了颈静脉、门静脉、肝静脉和颈动脉导管，以及肝动脉和门静脉血流袖带，用于测定经肝动力学和胰岛素分泌。三天后，以15微克/千克/小时的速度给它们输注大肠杆菌内毒素。在短暂的高胰岛素血症之前，由[6-3H]葡萄糖比活性测定的葡萄糖摄取率（Rd）升高。这一发现表明，高胰岛素血症可能是由Rd增加引起的，然后又促成了Rd的增加。如果胰岛β细胞也经历了葡萄糖摄取增加，现有的血糖状态可能会被高估，并引发不适当的胰岛素释放。
