Kleinbaum J, Shamoon H
Diabetes. 1983 Jun;32(6):493-8. doi: 10.2337/diab.32.6.493.
We evaluated the recovery of blood glucose after insulin-induced hypoglycemia in six insulin-dependent diabetics (insulin-infused and initially euglycemic) and six normal controls after comparable reductions in plasma glucose. In contrast to controls, the recovery of plasma glucose was delayed in diabetics (2-h plasma glucose 80 +/- 5 mg/dl and 58 +/- 5 mg/dl, respectively, P less than 0.01). This delay was due to the absence of a rebound in hepatic glucose output in the diabetics, whereas glucose output rose two- to threefold above baseline in normals. The impaired rebound in glucose output in diabetics could not be attributed to hyperinsulinemia. Rather, hypoglycemia-induced secretion of epinephrine and glucagon was reduced in the diabetics by 60-80% as compared with normals (P less than 0.001). The diabetics did not suffer from overt neuropathy and plasma cortisol, growth hormone, and norepinephrine increased normally following hypoglycemia. The data suggest that prolonged hypoglycemia may frequently occur in tightly controlled type I diabetics because of impaired rebound in hepatic glucose release which in turn may be a consequence of reduced secretion of epinephrine and glucagon.
我们评估了6名胰岛素依赖型糖尿病患者（通过输注胰岛素且初始血糖正常）和6名正常对照者在血浆葡萄糖可比降低后胰岛素诱导低血糖后的血糖恢复情况。与对照组相比，糖尿病患者的血浆葡萄糖恢复延迟（2小时血浆葡萄糖分别为80±5mg/dl和58±5mg/dl，P<0.01）。这种延迟是由于糖尿病患者肝葡萄糖输出没有出现反弹，而正常情况下葡萄糖输出比基线升高两到三倍。糖尿病患者葡萄糖输出的反弹受损不能归因于高胰岛素血症。相反，与正常对照者相比，糖尿病患者低血糖诱导的肾上腺素和胰高血糖素分泌减少了60-80%（P<0.001）。糖尿病患者没有明显的神经病变，低血糖后血浆皮质醇、生长激素和去甲肾上腺素正常增加。数据表明，在严格控制的I型糖尿病患者中，由于肝葡萄糖释放的反弹受损，可能经常发生长时间低血糖，而这反过来可能是肾上腺素和胰高血糖素分泌减少的结果。
