Insulin Reciprocally Regulates Glucagon Secretion in Humans
Insulin Reciprocally Regulates Glucagon Secretion in Humans
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DOI：
10.2337/db10-0728
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发表时间：
2010-11-01
期刊：
影响因子：
7.7
通讯作者：
Cryer, Philip E.
中科院分区：
文献类型：
--
作者：
Cooperberg, Benjamin A.;Cryer, Philip E.
我们测试了胰岛素本身增加的假设，即，在没有锌的情况下，抑制胰高血糖素分泌过程中的血糖正常，而胰岛素本身的减少刺激胰高血糖素分泌过程中的低血糖症在human.Research设计和方法我们测量血浆胰高血糖素浓度的1型糖尿病患者输注无锌谷赖胰岛素三次。在所有三种情况下，从0至60分钟输注谷赖氨酰胺和钳夹的欧替洛尔（类似于95 mg/dl [5.3 mmol/l]）。然后，停用谷赖胰岛素，同时钳夹血糖或钳夹低血糖结果血浆胰高血糖素浓度分别为-13 +/- 3、-9 +/- 3和-12 +/- 2 pg/ml，（-3.7 +/- 0.9、-2.6 +/- 0.9和-3.4 +/- 0.6 pmol/l），（所有P < 0.01）在前60分钟内无锌高胰岛素血症的eutrophin。胰高血糖素水平仍然受到抑制后，无锌胰岛素与eutrophin减少（-14 +/- 3 pg/ml [-4.0 +/- 0.9 pmol/l]）和持续高胰岛素血症伴低血糖期间（-14 +/- 2 pg/ml [-4.0 +/- 0.6 pmol/l]），但增加至-3 +/- 3 pg/ml（-0.9 +/- 0.9 pmol/l）（P < 0.01）。结论这些数据表明，胰岛素本身的增加抑制胰高血糖素分泌，而胰岛素本身的减少，与低葡萄糖浓度一致，刺激胰高血糖素分泌。因此，他们证明胰岛素是一种β细胞分泌产物，与葡萄糖和其他信号一起，可调节人类α细胞胰高血糖素分泌。糖尿病59：2936-2940，2010
OBJECTIVE-We tested the hypothesis that an increase in insulin per se, i.e., in the absence of zinc, suppresses glucagon secretion during euglycemia and that a decrease in insulin per se stimulates glucagon secretion during hypoglycemia in humans.RESEARCH DESIGN AND METHODS We measured plasma glucagon concentrations in patients with type 1 diabetes infused with the zinc-free insulin glulisine on three occasions. Glulisine was infused with clamped euglycemia (similar to 95 mg/dl [5.3 mmol/l]) from 0 to 60 min on all three occasions. Then, glulisine was discontinued with clamped euglycemia or with clamped hypoglycemia (similar to 55 mg/dl [3.0 mmol/l]) or continued with clamped hypoglycemia from 60 to 180 min.RESULTS Plasma glucagon concentrations were suppressed by -13 +/- 3, -9 +/- 3, and -12 +/- 2 pg/ml (-3.7 +/- 0.9, -2.6 +/- 0.9, and -3.4 +/- 0.6 pmol/l), respectively, (all P < 0.01) during zinc-free hyperinsulinemic euglycemia over the first 60 min. Glucagon levels remained suppressed following a decrease in zinc-free insulin with euglycemia (-14 +/- 3 pg/ml [-4.0 +/- 0.9 pmol/l]) and during sustained hyperinsulinemia with hypoglycemia (-14 +/- 2 pg/ml [-4.0 +/- 0.6 pmol/l]) but increased to -3 +/- 3 pg/ml (-0.9 +/- 0.9 pmol/l) (P < 0.01) following a decrease in zinc-free insulin with hypoglycemia over the next 120 min.CONCLUSIONS These data indicate that an increase in insulin per se suppresses glucagon secretion and a decrease in insulin per se, in concert with a low glucose concentration, stimulates glucagon secretion. Thus, they document that insulin is a beta-cell secretory product that, in concert with glucose and among other signals, reciprocally regulates a-cell glucagon secretion in humans. Diabetes 59:2936-2940, 2010