Sleep-related hypoglycemia-associated autonomic failure in type 1 diabetes - Reduced awakening from sleep during hypoglycemia
Sleep-related hypoglycemia-associated autonomic failure in type 1 diabetes - Reduced awakening from sleep during hypoglycemia
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DOI：
10.2337/diabetes.52.5.1195
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发表时间：
2003-05-01
期刊：
影响因子：
7.7
通讯作者：
Cryer, PE
中科院分区：
文献类型：
--
作者：
Banarer, S;Cryer, PE
鉴于医源性低血糖经常发生在 1 型糖尿病患者的夜间，我们测试了这样的假设：在 1 型糖尿病患者的睡眠期间，针对低血糖的生理和行为防御机制（已经因胰高血糖素缺失、肾上腺素减弱和神经源性症状反应而受到损害）进一步受到损害。为此，我们研究了 8 名患有无并发症的 1 型糖尿病的成年患者和 8 名匹配的非糖尿病对照受试者，这些受试者在早上 (0730-1230) 清醒时和夜间 (2100-0200) 清醒时和从 0000 点开始睡眠时使用高胰岛素阶梯式降血糖钳夹（血糖步长类似于 85、75、65、55 和 45 mg/dl）到 0200 以随机顺序。糖尿病受试者睡眠期间血浆肾上腺素 (P = 0.0010)、可能是去甲肾上腺素 (P = 0.0838) 和胰多肽 (P = 0.0034) 对低血糖的反应降低（最终的清醒与睡眠值分别为 240 86 和 85 47、205 24 和 148 17、197 +/- 45 和分别为 118 +/- 31 pg/ml），但在对照受试者中则不然。糖尿病受试者在低血糖期间从睡眠中醒来的时间明显减少。在 45 mg/dl 降血糖步骤后期，糖尿病受试者的睡眠效率（睡眠时间百分比）为 77 +/- 18%，但对照受试者仅为 26 +/- 8% (P = 0.0109)。我们得出的结论是，1 型糖尿病患者在睡眠期间对低血糖的自主反应减弱，并且可能由于交感肾上腺反应减弱，1 型糖尿病患者因低血糖而醒来的可能性大大降低。因此，生理和行为防御在睡眠期间都会进一步受到损害。在胰岛素替代不完善的情况下，这种与睡眠相关的低血糖相关的自主神经衰竭可能解释了 1 型糖尿病中夜间低血糖的高频率。
Given that iatrogenic hypoglycemia often occurs during the night in people with type 1 diabetes, we tested the hypothesis that physiological, and the resulting behavioral, defenses against developing hypoglycemia-already compromised by absent glucagon and attenuated epinephrine and neurogenic symptom responses-are further compromised during sleep in type 1 diabetes. To do so, we studied eight adult patients with uncomplicated type 1 diabetes and eight matched nondiabetic control subjects with hyperinsulinemic stepped hypo-glycemic clamps (glucose steps of similar to85, 75, 65, 55, and 45 mg/dl) in the morning (0730-1230) while awake and at night (2100-0200) while awake throughout and while asleep from 0000 to 0200 in random sequence. Plasma epinephrine (P = 0.0010), perhaps norepinephrine (P = 0.0838), and pancreatic polypeptide (P = 0.0034) responses to hypoglycemia were reduced during sleep in diabetic subjects (the final awake versus asleep values were 240 86 and 85 47, 205 24 and 148 17, and 197 +/- 45 and 118 +/- 31 pg/ml, respectively), but not in the control subjects. The diabetic subjects exhibited markedly reduced awakening from sleep during hypoglycemia. Sleep efficiency (percent time asleep) was 77 +/- 18% in the diabetic subjects, but only 26 +/- 8% (P = 0.0109) in the control subjects late in the 45-mg/dl hypoglycemic steps. We conclude that autonomic responses to hypoglycemia are reduced during sleep in type 1 diabetes, and that, probably because of their reduced sympathoadrenal responses, patients with type 1 diabetes are substantially less likely to be awakened by hypoglycemia. Thus both physiological and behavioral defenses are further compromised during sleep. This sleep-related hypoglycemia-associated autonomic failure, in the context of imperfect insulin replacement, likely explains the high frequency of nocturnal hypoglycemia in type 1 diabetes.