Hyperglycemia per se (insulin and glucagon withdrawn) can inhibit hepatic glucose production in man.
Hyperglycemia per se (insulin and glucagon withdrawn) can inhibit hepatic glucose production in man.
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高血糖本身（撤回胰岛素和胰高血糖素）可以抑制人类肝葡萄糖的产生。
DOI：
10.1210/jcem-48-1-171
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发表时间：
1979
期刊：
影响因子：
--
通讯作者：
D. Rabinowitz
中科院分区：
文献类型：
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作者：
J. Liljenquist;G. Mueller;A. Cherrington;J. Perry;D. Rabinowitz
我们检查了高血糖本身对净内脏葡萄糖平衡的影响。在接受肝静脉导管插入术的两组正常吸收后男性中，施用生长抑素以阻断内源性胰岛素和胰高血糖素分泌。两组均输注外源性葡萄糖，其中一组（n = 7）维持血糖正常2小时，第二组（n = 4）在血糖正常30分钟后诱导高血糖220-240 mg/dl。在两组中，在维持血糖正常的情况下诱导胰岛素减少和胰高血糖素减少，导致内脏葡萄糖净产生量 (NSGP) 最初下降 75%。在维持正常血糖的组中，NSGP 在 2 小时内恢复到基础速率（157 +/- 31 mg/min）。然而，在诱发高血糖的组中，NSGP 并未恢复至基础水平，而是在研究期间保持抑制状态（28 +/- 4 毫克/分钟）。正常人的这些数据表明，急剧撤回胰岛素和胰高血糖素引起的高血糖本身可以抑制内脏葡萄糖的产生，但不会诱导净内脏葡萄糖储存。
We examined the effect of hyperglycemia per se on net splanchnic glucose balance. In 2 groups of normal postabsorptive men who had undergone hepatic vein catheterization, somatostatin was administered to block endogenous insulin and glucagon secretion. Exogenous glucose was infused in both groups to maintain euglycemia for 2 h in one group (n = 7) and to induce hyperglycemia of 220-240 mg/dl after 30 minutes of euglycemia in the second group (n = 4). In both groups the induction of insulinopenia and glucagonopenia with euglycemia maintained resulted in an initial 75% fall in net splanchnic glucose production (NSGP). In the group in which euglycemia was maintained NSGP returned to basal rates (157 +/- 31 mg/min) within 2 h. However, in the group in which hyperglycemia was induced, NSGP did not return to basal rates but remained suppressed (28 +/- 4 mg/min) for the duration of the study. These data in normal man indicate that hyperglycemia per se with insulin and glucagon acutely withdrawn can suppress splanchnic glucose production but does not induce net splanchnic glucose storage.