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Four nights of sleep restriction suppress the postprandial lipemic response and decrease satiety

机译:四晚的睡眠限制抑制了餐后脂质反应并减少饱腹感

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Chronic sleep restriction, or inadequate sleep, is associated with increased risk of cardiometabolic disease. Laboratory studies demonstrate that sleep restriction causes impaired whole-body insulin sensitivity and glucose disposal. Evidence suggests that inadequate sleep also impairs adipose tissue insulin sensitivity and the NEFA rebound during intravenous glucose tolerance tests, yet no studies have examined the effects of sleep restriction on high-fat meal lipemia. We assessed the effect of 5 h time in bed (TIB) per night for four consecutive nights on postprandial lipemia following a standardized high-fat dinner (HFD). Furthermore, we assessed whether one night of recovery sleep (10 h TIB) was sufficient to restore postprandial metabolism to baseline. We found that postprandial triglyceride (TG) area under the curve was suppressed by sleep restriction (P = 0.01), but returned to baseline values following one night of recovery. Sleep restriction decreased NEFAs throughout the HFD (P = 0.02) and NEFAs remained suppressed in the recovery condition (P = 0.04). Sleep restriction also decreased participant-reported fullness or satiety (P = 0.03), and decreased postprandial interleukin-6 (P < 0.01). Our findings indicate that four nights of 5 h TIB per night impair postprandial lipemia and that one night of recovery sleep may be adequate for recovery of TG metabolism, but not for markers of adipocyte function.
机译:慢性睡眠限制或睡眠不足,与心细素疾病的风险增加有关。实验室研究表明,睡眠限制导致全身胰岛素敏感性和葡萄糖处理受损。证据表明,睡眠不足也损害了脂肪组织胰岛素敏感性和Nefa反弹,但没有研究睡眠限制对高脂膳食脂质血症的影响。在标准化高脂晚餐(HFD)后,我们评估了每晚5小时床(TIB)每晚床(TIB)的效果。此外,我们评估了一晚的恢复睡眠(10小时TIB)是否足以将餐后代谢恢复到基线。我们发现曲线下的后甘油三酯(TG)面积被睡眠限制抑制(P = 0.01),但在一夜恢复后返回基线值。睡眠限制在整个HFD(P = 0.02)中的NEFA减少(P = 0.02),并且在恢复条件下保持抑制NEFA(P = 0.04)。睡眠限制也降低了参与者报告的丰满或饱腹感(P = 0.03),并且减少的餐后白细胞介素-6(P <0.01)。我们的研究结果表明,每晚4晚5岁的晚上损害餐后脂质症,并且一夜恢复睡眠可能足以恢复TG代谢,但不适用于脂肪细胞功能的标记。

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