Levy C J, Kinsley B T, Bajaj M, Simonson D C
Joslin Diabetes Center, Boston, Massachusetts, USA.
Diabetes Care. 1998 Aug;21(8):1330-8. doi: 10.2337/diacare.21.8.1330.
We examined the effect of glycemic control of NIDDM on counterregulatory hormone responses to hypoglycemia and compared the effect with that seen in patients with IDDM.
Eleven subjects with NIDDM and eight age- and weight-matched control subjects and ten subjects with IDDM and ten age- and weight-matched control subjects were studied. All subjects underwent a stepped hypoglycemic-hyper-insulinemic clamp study during which plasma glucose levels were lowered in a stepwise manner from 5.0 to 2.2 mmol/l in steps of 0.6 mmol/l every 30 min. Counterregulatory hormones (epinephrine, norepinephrine, glucagon, ACTH, cortisol, and growth hormone [GH]) were measured, and a symptom survey was administered during the last 10 min of each 30-min interval.
The threshold for release of epinephrine, norepinephrine, ACTH, and cortisol occurred at higher plasma glucose levels in NIDDM than in IDDM patients (P < 0.05-0.01). The glucose threshold for release of epinephrine and norepinephrine correlated with glycemic control as measured by glycosylated hemoglobin (P < 0.05-0.01). However, for a given level of glycemic control, the threshold for release of epinephrine and norepinephrine occurred at a higher glucose level in NIDDM versus IDDM patients (P < 0.05-0.01). At the nadir level of hypoglycemia, glucagon, ACTH, and cortisol levels were all higher in NIDDM compared with IDDM subjects, whereas GH levels were lower.
Glycemic control alters counterregulatory responses to hypoglycemia in NIDDM as has been previously reported in IDDM. However, at similar levels of glycemic control, NIDDM patients release counterregulatory hormones at a higher plasma glucose level than patients with IDDM. In addition, subjects with NIDDM maintain their glucagon response to hypoglycemia. These data suggest that patients with NIDDM may be at reduced risk of severe hypoglycemia when compared with a group of IDDM patients in similar glycemic control, thus providing a more favorable risk-benefit ratio for intensive diabetes therapy in NIDDM.
我们研究了非胰岛素依赖型糖尿病（NIDDM）患者血糖控制对低血糖时升糖激素反应的影响，并将其与胰岛素依赖型糖尿病（IDDM）患者的情况进行比较。
对11例NIDDM患者、8例年龄和体重匹配的对照者、10例IDDM患者以及10例年龄和体重匹配的对照者进行了研究。所有受试者均接受了逐步低血糖-高胰岛素钳夹试验，在此期间，血浆葡萄糖水平每30分钟以0.6 mmol/L的步长从5.0 mmol/L逐步降至2.2 mmol/L。测量了升糖激素（肾上腺素、去甲肾上腺素、胰高血糖素、促肾上腺皮质激素、皮质醇和生长激素[GH]），并在每个30分钟间隔的最后10分钟进行了症状调查。
NIDDM患者肾上腺素、去甲肾上腺素、促肾上腺皮质激素和皮质醇释放的阈值出现在比IDDM患者更高的血浆葡萄糖水平时（P<0.05 - 0.01）。肾上腺素和去甲肾上腺素释放的葡萄糖阈值与糖化血红蛋白测量的血糖控制情况相关（P<0.05 - 0.01）。然而，对于给定的血糖控制水平，NIDDM患者肾上腺素和去甲肾上腺素释放的阈值出现在比IDDM患者更高的葡萄糖水平时（P<0.05 - 0.01）。在低血糖的最低点，NIDDM患者的胰高血糖素、促肾上腺皮质激素和皮质醇水平均高于IDDM受试者，而GH水平较低。
如先前在IDDM中所报道的，血糖控制会改变NIDDM患者对低血糖的升糖反应。然而，在相似的血糖控制水平下，NIDDM患者在更高的血浆葡萄糖水平时释放升糖激素。此外，NIDDM受试者维持其对低血糖的胰高血糖素反应。这些数据表明，与血糖控制相似的IDDM患者组相比，NIDDM患者发生严重低血糖的风险可能降低，从而为NIDDM强化糖尿病治疗提供了更有利的风险效益比。
