2012年10月16日 讯 /生物谷BIOON/ --在一项最新研究中，科学家挑战了长期固有的一个概念即睡眠功能只有大脑才有，研究人员发现没有得到足够“睡眠”的脂肪细胞会产生一定的有害影响，他们对胰岛素激素的反应能力减少了30％。
长期剥夺睡眠一直与大脑功能受损，导致警觉性和认知能力下降有关。芝加哥医学院的研究人员最新发现睡眠缺失与人类能量调节的破坏有关，随着时间的推移睡眠缺失可能会导致体重增加，引发糖尿病和其他健康问题。这项新研究表明睡眠在能量代谢中至少是很重要的，相关研究论文发表在10月16日的Annals of Internal Medicine杂志上。
研究报告的作者、美国芝加哥大学分子代谢和营养委员会Matthew Brady博士说：我们发现脂肪细胞需要正常“睡眠”。Brady表示身体脂肪在人体中起着重要的作用。身体脂肪也被称为脂肪组织，主要用于存储和释放能量。在存储模式下，脂肪细胞从血液循环中移除脂肪酸和脂肪，以免这些物质损坏其他组织。当脂肪细胞不能有效的响应胰岛素，这些脂类物质会浸出血液循环，导致严重的并发症。
芝加哥大学Esra Tasali医学博士等人招募了六名男子和一名女子，这些人均年轻、体重瘦，身体健康。每位志愿者都通过两个阶段的学习期，这两个学习期相隔至少4周。其中一组人每晚有8.5小时的睡眠时间，共持续4周。另一组只有 4.5个小时睡眠。两种条件下，严格控制受试者食物的摄入量。
在第四天晚上结束后的早晨起床时，每个志愿者进行静脉葡萄糖耐量试验，测量身体对胰岛素的敏感性。研究人员还进行了活检，从每个志愿者的腹部附近获得脂肪细胞，测量了这些脂肪细胞对胰岛素的敏感性。
研究人员通过测量脂肪细胞内Akt蛋白质的磷酸化水平评估胰岛素敏感性。在分子水平上， Akt的磷酸化是细胞对胰岛素的一个关键早期化学反应步骤。经历四晚短暂睡眠后的人，身体对胰岛素的反应平均下降16％，脂肪细胞对胰岛素的敏感性降低了30％。他们发现，只有提高近3倍的胰岛素水平才能激起睡眠缺失的人产生最大Akt的响应。
这项研究证实睡眠时间减少可能会直接促进糖尿病和肥胖等疾病发展，研究结果指出睡眠对身体机能包括代谢、脂肪组织、心血管功能等可能存在更多更广泛的影响。这项研究工作的经费来自国家健康与社会科学学院布兰科魏斯奖学金。（生物谷：Bioon.com）
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Impaired Insulin Signaling in Human Adipocytes After Experimental Sleep Restriction: A Randomized, Crossover Study
Josiane L. Broussard, David A. Ehrmann, Eve Van Cauter, Esra Tasali, Matthew J. Brady
Background: 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.
Objective: 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.
Design: Randomized, 2-period, 2-condition, crossover clinical study.
Setting: University of Chicago Clinical Resource Center.
Participants: 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/m2 (SD, 1.6).
Intervention: Four days of 4.5 hours in bed or 8.5 hours in bed under controlled conditions of caloric intake and physical activity.
Measurements: 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.
Results: 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.
Limitation: This was a single-center study with a small sample size.
Conclusion: Sleep restriction results in an insulin-resistant state in human adipocytes. Sleep may be an important regulator of energy metabolism in peripheral tissues.
