Jones T W, Porter P, Sherwin R S, Davis E A, O'Leary P, Frazer F, Byrne G, Stick S, Tamborlane W V
Department of Diabetes and Endocrinology, Princess Margaret Hospital for Children, Perth, WA, Australia.
N Engl J Med. 1998 Jun 4;338(23):1657-62. doi: 10.1056/NEJM199806043382303.
In patients with type I diabetes mellitus, hypoglycemia occurs commonly during sleep and is frequently asymptomatic. This raises the question of whether sleep is associated with reduced counterregulatory-hormone responses to hypoglycemia.
We studied the counterregulatory-hormone responses to insulin-induced hypoglycemia in eight adolescent patients with type I diabetes and six age-matched normal subjects when they were awake during the day, asleep at night, and awake at night. In each study, the plasma glucose concentration was stabilized for 60 minutes at approximately 100 mg per deciliter (5.6 mmol per liter) and then reduced to 50 mg per deciliter (2.8 mmol per liter) and maintained at that concentration for 40 minutes. Plasma free insulin, epinephrine, norepinephrine, cortisol, and growth hormone were measured frequently during each study. Sleep was monitored by polysomnography.
The plasma glucose and free insulin concentrations were similar in both groups during all studies. During the studies when the subjects were asleep, no one was awakened during the hypoglycemic phase, but during the final 30 minutes of the studies when the subjects were awake both the patients with diabetes and the normal subjects had symptoms of hypoglycemia. In the patients with diabetes, plasma epinephrine responses to hypoglycemia were blunted when they were asleep (mean [+/-SE] peak plasma epinephrine concentration, 70+/-14 pg per milliliter [382+/-76 pmol per liter]; P=0.3 for the comparison with base line), as compared with when they were awake during the day or night (238+/-39 pg per milliliter [1299+/-213 pmol per liter] P=0.004 for the comparison with base line, and 296+/-60 pg per milliliter [1616+/-327 pmol per liter], P=0.004, respectively). The patients' plasma norepinephrine responses were also reduced during sleep, whereas their plasma cortisol concentrations did not increase and their plasma growth hormone concentrations increased slightly. The patterns of counterregulatory-hormone responses in the normal subjects were similar.
Sleep impairs counterregulatory-hormone responses to hypoglycemia in patients with diabetes and normal subjects.
在1型糖尿病患者中,低血糖常见于睡眠期间,且常常无症状。这就引发了一个问题,即睡眠是否与低血糖时的反调节激素反应减弱有关。
我们研究了8名青少年1型糖尿病患者和6名年龄匹配的正常受试者在白天清醒、夜间睡眠和夜间清醒时对胰岛素诱导的低血糖的反调节激素反应。在每项研究中,血浆葡萄糖浓度在约每分升100毫克(每升5.6毫摩尔)稳定60分钟,然后降至每分升50毫克(每升2.8毫摩尔)并维持该浓度40分钟。在每项研究期间频繁测量血浆游离胰岛素、肾上腺素、去甲肾上腺素、皮质醇和生长激素。通过多导睡眠图监测睡眠情况。
在所有研究中,两组的血浆葡萄糖和游离胰岛素浓度相似。在受试者睡眠期间的研究中,低血糖阶段无人被唤醒,但在研究的最后30分钟,当受试者清醒时,糖尿病患者和正常受试者均出现低血糖症状。在糖尿病患者中,与白天或夜间清醒时相比,他们睡眠时血浆肾上腺素对低血糖的反应减弱(平均[±标准误]血浆肾上腺素峰值浓度,每毫升70±14皮克[每升382±76皮摩尔];与基线比较,P = 0.3),白天清醒时为每毫升238±39皮克[每升1299±213皮摩尔],与基线比较,P = 0.004,夜间清醒时为每毫升296±60皮克[每升1616±327皮摩尔],P = 0.004)。患者睡眠期间血浆去甲肾上腺素反应也降低,而血浆皮质醇浓度未升高,血浆生长激素浓度略有升高。正常受试者的反调节激素反应模式相似。
睡眠会损害糖尿病患者和正常受试者对低血糖的反调节激素反应。