Shaw Natalie D, McHill Andrew W, Schiavon Michele, Kangarloo Tairmae, Mankowski Piotr W, Cobelli Claudio, Klerman Elizabeth B, Hall Janet E
Reproductive Endocrine Unit, Department of Medicine, Massachusetts General Hospital, Boston, MA.
Clinical Research Branch, National Institute of Environmental Health Sciences (NIEHS), Research Triangle Park, NC.
Sleep. 2016 Aug 1;39(8):1591-9. doi: 10.5665/sleep.6028.
Cross-sectional studies report a correlation between slow wave sleep (SWS) duration and insulin sensitivity (SI) in children and adults. Suppression of SWS causes insulin resistance in adults but effects in children are unknown. This study was designed to determine the effect of SWS fragmentation on SI in children.
Fourteen pubertal children (11.3-14.1 y, body mass index 29(th) to 97(th) percentile) were randomized to sleep studies and mixed meal (MM) tolerance tests with and without SWS disruption. Beta-cell responsiveness (Φ) and SI were determined using oral minimal modeling.
During the disruption night, auditory stimuli (68.1 ± 10.7/night; mean ± standard error) decreased SWS by 40.0 ± 8.0%. SWS fragmentation did not affect fasting glucose (non-disrupted 76.9 ± 2.3 versus disrupted 80.6 ± 2.1 mg/dL), insulin (9.2 ± 1.6 versus 10.4 ± 2.0 μIU/mL), or C-peptide (1.9 ± 0.2 versus 1.9 ± 0.1 ng/mL) levels and did not impair SI (12.9 ± 2.3 versus 10.1 ± 1.6 10(-4) dL/kg/min per μIU/mL) or Φ (73.4 ± 7.8 versus 74.4 ± 8.4 10(-9) min(-1)) to a MM challenge. Only the subjects in the most insulin-sensitive tertile demonstrated a consistent decrease in SI after SWS disruption.
Pubertal children across a range of body mass indices may be resistant to the adverse metabolic effects of acute SWS disruption. Only those subjects with high SI (i.e., having the greatest "metabolic reserve") demonstrated a consistent decrease in SI. These results suggest that adolescents may have a unique ability to adapt to metabolic stressors, such as acute SWS disruption, to maintain euglycemia. Additional studies are necessary to confirm that this resiliency is maintained in settings of chronic SWS disruption.
横断面研究报告了儿童和成人的慢波睡眠（SWS）时长与胰岛素敏感性（SI）之间的相关性。抑制成人的慢波睡眠会导致胰岛素抵抗，但对儿童的影响尚不清楚。本研究旨在确定慢波睡眠片段化对儿童胰岛素敏感性的影响。
14名青春期儿童（11.3 - 14.1岁，体重指数处于第29至97百分位）被随机分配进行睡眠研究以及在有和没有慢波睡眠干扰的情况下进行混合餐（MM）耐量试验。使用口服最小模型确定β细胞反应性（Φ）和胰岛素敏感性。
在干扰夜间，听觉刺激（68.1±10.7次/夜；平均值±标准误）使慢波睡眠减少了40.0±8.0%。慢波睡眠片段化不影响空腹血糖（未受干扰时为76.9±2.3，受干扰时为80.6±2.1mg/dL）、胰岛素（9.2±1.6对10.4±2.0μIU/mL）或C肽（1.9±0.2对1.9±0.1ng/mL）水平，并且不损害对混合餐挑战的胰岛素敏感性（12.9±2.3对10.1±1.6 10⁻⁴dL/kg/min per μIU/mL）或β细胞反应性（73.4±7.8对74.4±8.4 10⁻⁹min⁻¹）。只有胰岛素敏感性最高的三分位数组中的受试者在慢波睡眠干扰后胰岛素敏感性出现持续下降。
一系列体重指数的青春期儿童可能对急性慢波睡眠干扰的不良代谢影响具有抗性。只有那些胰岛素敏感性高的受试者（即具有最大“代谢储备”的受试者）表现出胰岛素敏感性的持续下降。这些结果表明，青少年可能具有独特的能力来适应代谢应激源，如急性慢波睡眠干扰，以维持血糖正常。需要进一步研究来证实这种恢复力在慢性慢波睡眠干扰情况下是否得以维持。
