University of Chicago, Chicago, IL 60637, USA.
Ann Intern Med. 2012 Oct 16;157(8):549-57. doi: 10.7326/0003-4819-157-8-201210160-00005.
Insufficient sleep increases the risk for insulin resistance, type 2 diabetes, and obesity, suggesting that sleep restriction may impair peripheral metabolic pathways. Yet, a direct link between sleep restriction and alterations in molecular metabolic pathways in any peripheral human tissue has not been shown.
To determine whether sleep restriction results in reduced insulin sensitivity in subcutaneous fat, a peripheral tissue that plays a pivotal role in energy metabolism and balance.
Randomized, 2-period, 2-condition, crossover clinical study.
University of Chicago Clinical Resource Center.
Seven healthy adults (1 woman, 6 men) with a mean age of 23.7 years (SD, 3.8) and mean body mass index of 22.8 kg/m(2) (SD, 1.6).
Four days of 4.5 hours in bed or 8.5 hours in bed under controlled conditions of caloric intake and physical activity.
Adipocytes collected from subcutaneous fat biopsy samples after normal and restricted sleep conditions were exposed to incremental insulin concentrations. The ability of insulin to increase levels of phosphorylated Akt (pAkt), a crucial step in the insulin-signaling pathway, was assessed. Total Akt (tAkt) served as a loading control. The insulin concentration for the half-maximal stimulation of the pAkt-tAkt ratio was used as a measure of cellular insulin sensitivity. Total body insulin sensitivity was assessed using a frequently sampled intravenous glucose tolerance test.
The insulin concentration for the half-maximal pAkt-tAkt response was nearly 3-fold higher (mean, 0.71 nM [SD, 0.27] vs. 0.24 nM [SD, 0.24]; P = 0.01; mean difference, 0.47 nM [SD, 0.33]; P = 0.01), and the total area under the receiver-operating characteristic curve of the pAkt-tAkt response was 30% lower (P = 0.01) during sleep restriction than during normal sleep. A reduction in total body insulin sensitivity (P = 0.02) paralleled this impaired cellular insulin sensitivity.
This was a single-center study with a small sample size.
Sleep restriction results in an insulin-resistant state in human adipocytes. Sleep may be an important regulator of energy metabolism in peripheral tissues.
National Institutes of Health.
睡眠不足会增加胰岛素抵抗、2 型糖尿病和肥胖的风险，这表明睡眠限制可能会损害外周代谢途径。然而，睡眠限制与任何外周人体组织中分子代谢途径的改变之间的直接联系尚未得到证实。
确定睡眠限制是否会导致皮下脂肪的胰岛素敏感性降低，皮下脂肪是能量代谢和平衡中起关键作用的外周组织。
随机、2 期、2 条件、交叉临床试验。
芝加哥大学临床资源中心。
7 名健康成年人（1 名女性，6 名男性），平均年龄 23.7 岁（标准差，3.8），平均体重指数为 22.8kg/m²（标准差，1.6）。
在控制热量摄入和体力活动的条件下，4.5 小时卧床或 8.5 小时卧床 4 天。
正常和限制睡眠条件下采集的皮下脂肪活检样本中的脂肪细胞，然后暴露于递增的胰岛素浓度下。评估胰岛素增加磷酸化 Akt（pAkt）水平的能力，pAkt 是胰岛素信号通路中的关键步骤。总 Akt（tAkt）用作加载对照。胰岛素浓度的一半可最大刺激 pAkt-tAkt 比值，作为细胞胰岛素敏感性的衡量标准。使用频繁采样静脉葡萄糖耐量试验评估全身胰岛素敏感性。
半最大 pAkt-tAkt 反应的胰岛素浓度高近 3 倍（平均值，0.71nM[标准差，0.27]vs.0.24nM[标准差，0.24]；P=0.01；平均差异，0.47nM[标准差，0.33]；P=0.01），并且 pAkt-tAkt 反应的总受试者工作特征曲线下面积低 30%（P=0.01）在睡眠限制期间比在正常睡眠期间。全身胰岛素敏感性的降低（P=0.02）与这种细胞胰岛素敏感性受损相平行。
这是一项单中心研究，样本量较小。
睡眠限制导致人体脂肪细胞出现胰岛素抵抗状态。睡眠可能是外周组织能量代谢的重要调节剂。
美国国立卫生研究院。
