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Sleep influences on obesity, insulin resistance, and risk of type 2 diabetes.睡眠对肥胖、胰岛素抵抗和 2 型糖尿病风险的影响。
Metabolism. 2018 Jul;84:56-66. doi: 10.1016/j.metabol.2018.02.010. Epub 2018 Mar 3.
2
Sleep Duration and Quality: Impact on Lifestyle Behaviors and Cardiometabolic Health: A Scientific Statement From the American Heart Association.睡眠时间与质量:对生活方式行为和心脏代谢健康的影响:美国心脏协会的科学声明
Circulation. 2016 Nov 1;134(18):e367-e386. doi: 10.1161/CIR.0000000000000444. Epub 2016 Sep 19.
3
Two Nights of Recovery Sleep Reverses the Effects of Short-term Sleep Restriction on Diabetes Risk.两晚的恢复性睡眠可逆转短期睡眠限制对糖尿病风险的影响。
Diabetes Care. 2016 Mar;39(3):e40-1. doi: 10.2337/dc15-2214. Epub 2016 Jan 19.
4
Model-Based Quantification of the Systemic Interplay between Glucose and Fatty Acids in the Postprandial State.基于模型的餐后状态下葡萄糖与脂肪酸之间全身相互作用的定量分析
PLoS One. 2015 Sep 10;10(9):e0135665. doi: 10.1371/journal.pone.0135665. eCollection 2015.
5
Elevated nocturnal NEFA are an early signal for hyperinsulinaemic compensation during diet-induced insulin resistance in dogs.夜间非酯化脂肪酸升高是犬类饮食诱导的胰岛素抵抗期间高胰岛素血症代偿的早期信号。
Diabetologia. 2015 Nov;58(11):2663-70. doi: 10.1007/s00125-015-3721-6. Epub 2015 Aug 9.
6
Sleep restriction increases free fatty acids in healthy men.睡眠限制会增加健康男性体内的游离脂肪酸。
Diabetologia. 2015 Apr;58(4):791-8. doi: 10.1007/s00125-015-3500-4. Epub 2015 Feb 22.
7
Fatty acid signaling: the new function of intracellular lipases.脂肪酸信号传导:细胞内脂肪酶的新功能。
Int J Mol Sci. 2015 Feb 10;16(2):3831-55. doi: 10.3390/ijms16023831.
8
Subchronic sleep restriction causes tissue-specific insulin resistance.亚慢性睡眠限制会导致组织特异性胰岛素抵抗。
J Clin Endocrinol Metab. 2015 Apr;100(4):1664-71. doi: 10.1210/jc.2014-3911. Epub 2015 Feb 6.
9
Interactions between sleep, circadian function, and glucose metabolism: implications for risk and severity of diabetes.睡眠、昼夜节律功能和葡萄糖代谢之间的相互作用:对糖尿病风险和严重程度的影响。
Ann N Y Acad Sci. 2014 Apr;1311:151-73. doi: 10.1111/nyas.12355. Epub 2014 Mar 14.
10
Dissecting adipose tissue lipolysis: molecular regulation and implications for metabolic disease.解析脂肪组织脂解:分子调控及其对代谢性疾病的影响。
J Mol Endocrinol. 2014 Jun;52(3):R199-222. doi: 10.1530/JME-13-0277. Epub 2014 Feb 27.

两晚的恢复性睡眠可恢复由五晚睡眠限制引起的动态血脂反应,但不能恢复胰岛素敏感性的降低。

Two nights of recovery sleep restores the dynamic lipemic response, but not the reduction of insulin sensitivity, induced by five nights of sleep restriction.

机构信息

The Huck Institutes of the Life Sciences, Pennsylvania State University , University Park, Pennsylvania.

Department of Biobehavioral Health, Pennsylvania State University , University Park, Pennsylvania.

出版信息

Am J Physiol Regul Integr Comp Physiol. 2019 Jun 1;316(6):R697-R703. doi: 10.1152/ajpregu.00336.2018. Epub 2019 Mar 20.

DOI:10.1152/ajpregu.00336.2018
PMID:30892916
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6620653/
Abstract

Chronic inadequate sleep is associated with increased risk of cardiometabolic diseases. The mechanisms involved are poorly understood but involve changes in insulin sensitivity, including within adipose tissue. The aim of this study was to assess the effects of sleep restriction on nonesterified fatty acid (NEFA) suppression profiles in response to an intravenous glucose tolerance test (IVGTT) and to assess whether 2 nights of recovery sleep (a "weekend") is sufficient to restore metabolic health. We hypothesized that sleep restriction impairs both glucose and lipid metabolism, specifically adipocyte insulin sensitivity, and the dynamic lipemic response of adipocyte NEFA release during an IVGTT. Fifteen healthy men completed an inpatient study of 3 baseline nights (10 h of time in bed/night), followed by 5 nights of 5 h of time in bed/night and 2 recovery nights (10 h of time in bed/night). IVGTTs were performed on the final day of each condition. Reductions in insulin sensitivity without a compensatory change in acute insulin response to glucose were consistent with prior studies (insulin sensitivity = 0.002; acute insulin response to glucose = 0.23). The disposition index was suppressed by sleep restriction and did not recover after recovery sleep ( < 0.0001 and = 0.01, respectively). Fasting NEFAs were not different from baseline in either the restriction or recovery conditions. NEFA rebound was significantly suppressed by sleep restriction ( = 0.01) but returned to baseline values after recovery sleep. Our study indicates that sleep restriction impacts NEFA metabolism and demonstrates that 2 nights of recovery sleep may not be adequate to restore glycemic health.

摘要

慢性睡眠不足与心血管代谢疾病风险增加有关。涉及的机制尚不清楚,但涉及胰岛素敏感性的变化,包括脂肪组织中的变化。本研究旨在评估睡眠限制对静脉葡萄糖耐量试验(IVGTT)中游离脂肪酸(NEFA)抑制谱的影响,并评估 2 个恢复性睡眠(“周末”)是否足以恢复代谢健康。我们假设睡眠限制会损害葡萄糖和脂质代谢,特别是脂肪细胞胰岛素敏感性,以及 IVGTT 期间脂肪细胞 NEFA 释放的动态血脂反应。15 名健康男性完成了 3 个基线夜间(每晚 10 小时卧床时间)的住院研究,随后进行了 5 个每晚 5 小时卧床时间和 2 个恢复性夜间(每晚 10 小时卧床时间)的研究。在每个条件的最后一天进行 IVGTT。胰岛素敏感性的降低而葡萄糖急性胰岛素反应没有代偿性变化与先前的研究一致(胰岛素敏感性= 0.002;急性胰岛素反应葡萄糖= 0.23)。处置指数受到睡眠限制的抑制,在恢复性睡眠后并未恢复(<0.0001 和= 0.01,分别)。限制或恢复条件下的空腹 NEFA 与基线相比没有差异。睡眠限制明显抑制了 NEFA 反弹(= 0.01),但在恢复性睡眠后恢复到基线值。我们的研究表明,睡眠限制会影响 NEFA 代谢,并表明 2 个恢复性睡眠可能不足以恢复血糖健康。