Danish Center for Sleep Medicine, Department of Clinical Neurophysiology, Copenhagen University Hospital, Glostrup, Denmark
Novo Nordisk A/S, Søborg, Denmark.
Diabetes Care. 2015 Nov;38(11):2151-7. doi: 10.2337/dc15-0907. Epub 2015 Sep 25.
The aim of this trial was to investigate the impact of nocturnal hypoglycemia on sleep patterns (assessed by polysomnography) and counterregulatory hormones.
In this single-blinded, crossover trial, 26 subjects with type 2 diabetes attended two experimental night visits (one normoglycemic and one hypoglycemic) in randomized order. Plasma glucose (PG) levels were controlled by hyperinsulinemic glucose clamping. On the hypoglycemic night, hypoglycemia was induced after reaching sleep stage N2 by turning off glucose infusion until the PG target of 2.7-2.8 mmol/L was reached and maintained for 15 min. Thereafter, subjects were brought back to normoglycemia for the rest of the night. On the normoglycemic night, PG was maintained at 5.0-7.0 mmol/L throughout the night.
During the first 4 h of sleep (0-4 h; after reaching sleep stage N2), no difference between experimental nights was observed in the rate of electroencephalography-identified arousals or awakenings, but the rate of awakenings was 27% lower during 4-8 h and 20% lower during 0-8 h on the hypoglycemic night than on the normoglycemic night (both statistically significant). Total sleep time tended to be longer on the hypoglycemic night (observed means 366 vs. 349 min, P nonsignificant). Statistically significantly higher counterregulatory hormonal responses (adrenaline, growth hormone, and cortisol) to hypoglycemia were observed compared with normoglycemia.
Nocturnal hypoglycemia in patients with type 2 diabetes caused a decrease in awakening response in the 4-8-h period following the event. These findings underscore the risks associated with nocturnal hypoglycemia because nocturnal hypoglycemia potentially affects the patient's ability to wake up and respond with an adequate intake of carbohydrates.
本试验旨在研究夜间低血糖对睡眠模式（通过多导睡眠图评估）和代偿性激素的影响。
在这项单盲、交叉试验中，26 名 2 型糖尿病患者以随机顺序接受了两次实验性夜间就诊（一次血糖正常，一次低血糖）。通过超胰岛素葡萄糖钳夹控制血浆葡萄糖（PG）水平。在低血糖夜间，当 PG 目标达到 2.7-2.8mmol/L 并维持 15min 时，通过关闭葡萄糖输注，使睡眠期 N2 后发生低血糖，然后将 PG 目标恢复到正常。在正常血糖夜间，PG 整晚维持在 5.0-7.0mmol/L。
在睡眠的前 4 小时（0-4 小时；达到睡眠阶段 N2 后），两个实验夜之间在脑电图识别的觉醒或唤醒率方面没有差异，但在低血糖夜的 4-8 小时和 0-8 小时期间，唤醒率分别降低了 27%和 20%（均具有统计学意义）。低血糖夜的总睡眠时间倾向于更长（观察到的平均值分别为 366 和 349min，P 无统计学意义）。与血糖正常相比，低血糖时观察到的代偿性激素反应（肾上腺素、生长激素和皮质醇）显著升高。
2 型糖尿病患者夜间低血糖导致事件后 4-8 小时内觉醒反应下降。这些发现强调了夜间低血糖相关的风险，因为夜间低血糖可能会影响患者醒来并通过摄入足够的碳水化合物来做出反应的能力。
