Influence of physiologic hyperglucagonemia on basal and insulin-inhibited splanchnic glucose output in normal man.
Influence of physiologic hyperglucagonemia on basal and insulin-inhibited splanchnic glucose output in normal man.
复制标题
生理性高胰高血糖素血症对正常人基础和胰岛素抑制内脏葡萄糖输出的影响。
DOI：
10.1172/jci108523
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发表时间：
1976
期刊：
影响因子：
--
通讯作者：
R. Hendler
中科院分区：
文献类型：
--
作者：
P. Felig;J. Wahren;R. Hendler
为评价生理性高血糖对内脏葡萄糖输出的影响，健康受试者在基础状态和内脏葡萄糖输出被葡萄糖抑制后(2 mg/kg/min)，分别以3 ng/kg/min的剂量输注胰高血糖素。在基础状态下，静脉注射高血糖素使血浆浓度升高309+/-25pg/ml，同时内脏葡萄糖输出量在7-15分钟内迅速增加到基础值的2-3倍。动脉血糖(0.5-1.5 mM)的升高与内脏葡萄糖输出量的增加直接相关。尽管持续输注胰高血糖素，面对稳定的胰岛素水平，内脏葡萄糖输出量在22分钟后下降，30-45分钟恢复到基础水平。在最初接受葡萄糖输注的受试者中，动脉胰岛素浓度上升了5-12MU/ml，而内脏葡萄糖输出量下降了85%-100%。静脉注射高血糖素使血浆高血糖素浓度增加272+/-30pg/ml，在5min内逆转内脏葡萄糖生成的抑制。内脏葡萄糖输出量在10min时比基础水平高出60%达到峰值，随后在30-45min下降到比基础水平低20%-25%。这些发现提供了直接的证据，证明血浆胰高血糖素的生理性增加刺激了基础状态的内脏葡萄糖输出，并逆转了胰岛素对内脏葡萄糖产生的抑制作用。胰高血糖素对内脏葡萄糖输出的刺激作用是短暂的，这表明抑制或逆转胰高血糖素的作用迅速发展。这种抑制似乎并不依赖于胰岛素分泌的增加。
To evaluate the effects of physiologic hyperglucagonemia on splanchnic glucose output, glucagon was infused in a dose of 3 ng/kg per min to healthy subjects in the basal state and after splanchnic glucose output had been inhibited by an infusion of glucose (2 mg/kg per min). In the basal state, infusion of glucagon causing a 309 +/- 25 pg/ml rise in plasma concentration was accompanied by a rapid increase in splanchnic glucose output to values two to three times basal by 7-15 min. The rise in arterial blood glucose (0.5-1.5 mM) correlated directly with the increment in splanchnic glucose output. Despite continued glucagon infusion, and in the face of stable insulin levels, splanchnic glucose output declined after 22 min, returning to basal levels by 30-45 min. In the subjects initially receiving the glucose infusion, arterial insulin concentration rose by 5-12 muU/ml, while splanchnic glucose output fell by 85-100%. Infusion of glucagon causing an increment in plasma glucagon concentration of 272 +/- 30 pg/ml reversed the inhibition in splanchnic glucose production within 5 min. Splanchnic glucose output reached a peak increment 60% above basal levels at 10 min, and subsequently declined to levels 20-25% below basal at 30-45 min. These findings provide direct evidence that physiologic increments in plasma glucagon stimulate splanchnic glucose output in the basal state and reverse insulin-mediated inhibition of splanchnic glucose production in normal man. The transient nature of the stimulatory effect of glucagon on splanchnic glucose output suggests the rapid development of inhibition or reversal of glucagon action. This inhibition does not appear to depend on increased insulin secretio.