2012年10月16日 訊 /生物谷BIOON/ --在一項(xiàng)最新研究中,，科學(xué)家挑戰(zhàn)了長(zhǎng)期固有的一個(gè)概念即睡眠功能只有大腦才有，研究人員發(fā)現(xiàn)沒(méi)有得到足夠“睡眠”的脂肪細(xì)胞會(huì)產(chǎn)生一定的有害影響,，他們對(duì)胰島素激素的反應(yīng)能力減少了30％,。
長(zhǎng)期剝奪睡眠一直與大腦功能受損，導(dǎo)致警覺(jué)性和認(rèn)知能力下降有關(guān),。芝加哥醫(yī)學(xué)院的研究人員最新發(fā)現(xiàn)睡眠缺失與人類能量調(diào)節(jié)的破壞有關(guān),，隨著時(shí)間的推移睡眠缺失可能會(huì)導(dǎo)致體重增加，引發(fā)糖尿病和其他健康問(wèn)題,。這項(xiàng)新研究表明睡眠在能量代謝中至少是很重要的,，相關(guān)研究論文發(fā)表在10月16日的Annals of Internal Medicine雜志上。
研究報(bào)告的作者,、美國(guó)芝加哥大學(xué)分子代謝和營(yíng)養(yǎng)委員會(huì)Matthew Brady博士說(shuō)：我們發(fā)現(xiàn)脂肪細(xì)胞需要正常“睡眠”,。Brady表示身體脂肪在人體中起著重要的作用,。身體脂肪也被稱為脂肪組織,，主要用于存儲(chǔ)和釋放能量。在存儲(chǔ)模式下，脂肪細(xì)胞從血液循環(huán)中移除脂肪酸和脂肪,，以免這些物質(zhì)損壞其他組織,。當(dāng)脂肪細(xì)胞不能有效的響應(yīng)胰島素，這些脂類物質(zhì)會(huì)浸出血液循環(huán),，導(dǎo)致嚴(yán)重的并發(fā)癥,。
芝加哥大學(xué)Esra Tasali醫(yī)學(xué)博士等人招募了六名男子和一名女子，這些人均年輕,、體重瘦,，身體健康。每位志愿者都通過(guò)兩個(gè)階段的學(xué)習(xí)期,，這兩個(gè)學(xué)習(xí)期相隔至少4周,。其中一組人每晚有8.5小時(shí)的睡眠時(shí)間，共持續(xù)4周,。另一組只有 4.5個(gè)小時(shí)睡眠,。兩種條件下，嚴(yán)格控制受試者食物的攝入量,。
在第四天晚上結(jié)束后的早晨起床時(shí),，每個(gè)志愿者進(jìn)行靜脈葡萄糖耐量試驗(yàn)，測(cè)量身體對(duì)胰島素的敏感性,。研究人員還進(jìn)行了活檢,，從每個(gè)志愿者的腹部附近獲得脂肪細(xì)胞，測(cè)量了這些脂肪細(xì)胞對(duì)胰島素的敏感性,。
研究人員通過(guò)測(cè)量脂肪細(xì)胞內(nèi)Akt蛋白質(zhì)的磷酸化水平評(píng)估胰島素敏感性,。在分子水平上， Akt的磷酸化是細(xì)胞對(duì)胰島素的一個(gè)關(guān)鍵早期化學(xué)反應(yīng)步驟,。經(jīng)歷四晚短暫睡眠后的人,，身體對(duì)胰島素的反應(yīng)平均下降16％，脂肪細(xì)胞對(duì)胰島素的敏感性降低了30％,。他們發(fā)現(xiàn),，只有提高近3倍的胰島素水平才能激起睡眠缺失的人產(chǎn)生最大Akt的響應(yīng)。
這項(xiàng)研究證實(shí)睡眠時(shí)間減少可能會(huì)直接促進(jìn)糖尿病和肥胖等疾病發(fā)展,，研究結(jié)果指出睡眠對(duì)身體機(jī)能包括代謝,、脂肪組織、心血管功能等可能存在更多更廣泛的影響,。這項(xiàng)研究工作的經(jīng)費(fèi)來(lái)自國(guó)家健康與社會(huì)科學(xué)學(xué)院布蘭科魏斯獎(jiǎng)學(xué)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.
