Chapotot F, Gronfier C, Spiegel K, Luthringer R, Brandenberger G
Laboratoire de Physiologie et de Psychologie Environnementales, CNRS, Strasbourg, France.
J Clin Endocrinol Metab. 1996 Oct;81(10):3759-65. doi: 10.1210/jcem.81.10.8855835.
To determine whether the 24-h intact PTH (iPTH) profile is influenced by the sleep-wake cycle, and whether iPTH pulses show a temporal relationship with internal sleep structure, eight normal young men were studied during 24 h under basal conditions, once with normal nighttime sleep from 2300-0700 h and once after a night of sleep deprivation followed by an 8-h period of daytime sleep from 0700-1500 h. During the 8-h nighttime sleep period, mean iPTH levels were significantly increased by +13% and mean iPTH pulse amplitudes by +31% as compared with the 8-h subsequent waking periods. During the 8 h of total sleep deprivation, mean iPTH levels were not significantly different from the corresponding period in nighttime sleep condition, but mean iPTH pulse amplitudes were significantly lower (P < 0.01). The 8-h daytime sleep period was associated with increased mean iPTH levels and mean iPTH pulse amplitudes (+15% and +57%, respectively, as compared with the corresponding period in nighttime sleep condition). The number of pulses was similar in both experimental series and was not influenced by sleep or by time of day. Analysis of coincidence between iPTH pulses, plasma ionized calcium and plasma phosphate pulses, and slow wave sleep, as well as with rapid eye movement sleep episodes, did not reveal any significant association. Cross-correlation analysis between iPTH, plasma ionized calcium, and plasma phosphate fluctuations during sleep also showed no systematic association. Seven other subjects were studied during a nighttime sleep period in which temporal relationships between iPTH and internal sleep structure were reevaluated using spectral analysis of the sleep electroencephalogram. Cross-correlation analysis between iPTH levels and delta-relative power fluctuations showed nonsignificant results, which confirms the lack of relationship with slow wave sleep. This study demonstrates that the iPTH 24-h profile is influenced by sleep processes with a weak circadian component. However, iPTH pulses are not temporally linked with sleep electroencephalographic activity nor with calcemia and phosphatemia fluctuations. This evidence raises questions about the origin of iPTH pulses.
为了确定24小时完整甲状旁腺激素（iPTH）谱是否受睡眠-觉醒周期影响，以及iPTH脉冲与内部睡眠结构是否存在时间关系，对8名正常年轻男性在基础条件下进行了24小时研究，一次是从23:00至07:00的正常夜间睡眠，另一次是经过一夜睡眠剥夺后，从07:00至15:00进行8小时的日间睡眠。在8小时夜间睡眠期间，与随后8小时的清醒期相比，平均iPTH水平显著升高13%，平均iPTH脉冲幅度升高31%。在完全睡眠剥夺的8小时内，平均iPTH水平与夜间睡眠条件下的相应时间段无显著差异，但平均iPTH脉冲幅度显著降低（P<0.01）。8小时的日间睡眠期与平均iPTH水平和平均iPTH脉冲幅度增加有关（与夜间睡眠条件下的相应时间段相比，分别增加15%和57%）。两个实验系列中的脉冲数量相似，且不受睡眠或一天中时间的影响。对iPTH脉冲、血浆离子钙和血浆磷酸盐脉冲以及慢波睡眠之间的一致性分析，以及与快速眼动睡眠发作的分析，均未发现任何显著关联。睡眠期间iPTH、血浆离子钙和血浆磷酸盐波动之间的互相关分析也未显示出系统关联。对另外7名受试者在夜间睡眠期间进行了研究，其中使用睡眠脑电图的频谱分析重新评估了iPTH与内部睡眠结构之间的时间关系。iPTH水平与δ相对功率波动之间的互相关分析结果不显著，这证实了与慢波睡眠缺乏关系。本研究表明，iPTH的24小时谱受睡眠过程影响，昼夜节律成分较弱。然而，iPTH脉冲与睡眠脑电图活动以及血钙和血磷波动在时间上并无关联。这一证据引发了关于iPTH脉冲起源的问题。
