ROLE OF INSULIN AND GLUCAGON IN REGULATION OF BASAL GLUCOSE PRODUCTION IN POSTABSORPTIVE DOG
ROLE OF INSULIN AND GLUCAGON IN REGULATION OF BASAL GLUCOSE PRODUCTION IN POSTABSORPTIVE DOG
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DOI：
10.1172/jci108596
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发表时间：
1976-01-01
影响因子：
15.9
通讯作者：
LACY, WW
中科院分区：
文献类型：
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作者：
CHERRINGTON, AD;CHIASSON, JL;LACY, WW
通过单独或与门静脉内替代输注任一胰腺激素的组合输注生长抑素(1μg/kg/分钟)来实现一种或两种胰腺激素的缺乏，生长抑素是胰岛素和胰高血糖素分泌的有效抑制剂。单独输注生长抑素导致动脉胰岛素和胰高血糖素水平迅速下降 72.+-。 6 和 81.+-。分别为 8%。分别以每分钟400μU[微单位]/kg和每分钟1ng/kg的速率门静脉内输注胰岛素和胰高血糖素维持每种激素的基础水平。使用示踪剂（[3-3H]葡萄糖的引发恒定输注）和动静脉差异技术测量葡萄糖的产生。孤立的胰高血糖素缺乏导致 35 .+-。葡萄糖产量快速持续下降 5%（P < 0.05），血浆胰高血糖素水平恢复后即被消除。孤立的胰岛素缺乏导致 52 .+-。葡萄糖生成率增加 16%（P < 0.01），但当胰岛素水平恢复时，葡萄糖生成率则消失。当同时门脉内输注胰岛素和胰高血糖素来阻止生长抑素通常引起的胰腺激素水平的变化时，生长抑素对葡萄糖的产生没有影响。在禁食过夜的麻醉犬中：基础胰高血糖素负责至少 1/3 的基础葡萄糖生成；基础胰岛素可防止因胰高血糖素不受限制的作用而导致的葡萄糖产生增加；生长抑素除了通过干扰胰腺激素分泌而引起的葡萄糖转换外，对葡萄糖转换没有急性影响。两种胰腺激素的相反作用对于吸收后状态下基础葡萄糖产生的调节很重要。
A deficiency of either or both pancreatic hormones was achieved by infusing somatostatin (1 .mu.g/kg per min), a potent inhibitor of both insulin and glucagon secretion, alone or in combination with intraportal replacement infusions of either pancreatic hormone. Infusion of somatostatin alone caused the arterial levels of insulin and glucagon to drop rapidly by 72 .+-. 6 and 81 .+-. 8%, respectively. Intraportal infusion of insulin and glucagon at rates of 400 .mu.U[microunits]/kg per min and 1 ng/kg per min, respectively, maintained the basal levels of each hormone. Glucose production was measured using tracer (primed constant infusion of [3-3H]glucose) and arteriovenous difference techniques. Isolated glucagon deficiency resulted in a 35 .+-. 5% (P < 0.05) rapid and sustained decrease in glucose production which was abolished upon restoration of the plasma glucagon level. Isolated insulin deficiency resulted in a 52 .+-. 16% (P < 0.01) increase in the rate of glucose production which was abolished when the insulin level was restored. Somatostatin had no effect on glucose production when the changes in the pancreatic hormone levels which it normally induces were prevented by simultaneous intraportal infusion of both insulin and glucagon. In the anesthetized dog fasted overnight: basal glucagon is responsible for at least 1/3 of basal glucose production; basal insulin prevents the increased glucose production which would result from the unrestrained action of glucagon; and somatostatin has no acute effects on glucose turnover other than those it induces through perturbation of pancreatic hormone secretion. The opposing actions of the 2 pancreatic hormones are important in the regulation of basal glucose production in the postabsorptive state.