Genetic & Molecular Epidemiology Unit, Lund University Diabetes Centre, Department of Clinical Sciences, Lund University, Malmö, Sweden.
Center for Human Sleep Science, Department of Psychology, University of California, Berkeley, CA, USA.
Diabetologia. 2022 Feb;65(2):356-365. doi: 10.1007/s00125-021-05608-y. Epub 2021 Nov 30.
AIMS/HYPOTHESIS: Sleep, diet and exercise are fundamental to metabolic homeostasis. In this secondary analysis of a repeated measures, nutritional intervention study, we tested whether an individual's sleep quality, duration and timing impact glycaemic response to a breakfast meal the following morning.
Healthy adults' data (N = 953 [41% twins]) were analysed from the PREDICT dietary intervention trial. Participants consumed isoenergetic standardised meals over 2 weeks in the clinic and at home. Actigraphy was used to assess sleep variables (duration, efficiency, timing) and continuous glucose monitors were used to measure glycaemic variation (>8000 meals).
Sleep variables were significantly associated with postprandial glycaemic control (2 h incremental AUC), at both between- and within-person levels. Sleep period time interacted with meal type, with a smaller effect of poor sleep on postprandial blood glucose levels when high-carbohydrate (low fat/protein) (p = 0.02) and high-fat (p = 0.03) breakfasts were consumed compared with a reference 75 g OGTT. Within-person sleep period time had a similar interaction (high carbohydrate: p = 0.001, high fat: p = 0.02). Within- and between-person sleep efficiency were significantly associated with lower postprandial blood glucose levels irrespective of meal type (both p < 0.03). Later sleep midpoint (time deviation from midnight) was found to be significantly associated with higher postprandial glucose, in both between-person and within-person comparisons (p = 0.035 and p = 0.051, respectively).
CONCLUSIONS/INTERPRETATION: Poor sleep efficiency and later bedtime routines are associated with more pronounced postprandial glycaemic responses to breakfast the following morning. A person's deviation from their usual sleep pattern was also associated with poorer postprandial glycaemic control. These findings underscore sleep as a modifiable, non-pharmacological therapeutic target for the optimal regulation of human metabolic health. Trial registration ClinicalTrials.gov NCT03479866.
目的/假设：睡眠、饮食和运动是代谢稳态的基础。在这项重复测量、营养干预研究的二次分析中，我们测试了个体的睡眠质量、时长和时间是否会影响第二天早餐后的血糖反应。
对 PREDICT 饮食干预试验中的健康成年人数据（N=953[41%为双胞胎]）进行了分析。参与者在诊所和家中的 2 周内摄入等能量标准餐。使用活动记录仪评估睡眠变量（时长、效率、时间），使用连续血糖监测仪测量血糖变化（>8000 餐）。
睡眠变量与餐后血糖控制（2 小时增量 AUC）在个体间和个体内水平均显著相关。睡眠时间与进餐类型相互作用，与高碳水化合物（低脂肪/蛋白质）（p=0.02）和高脂肪（p=0.03）早餐相比，较差的睡眠对餐后血糖水平的影响较小。个体内睡眠时间也有类似的相互作用（高碳水化合物：p=0.001，高脂肪：p=0.02）。无论进餐类型如何，个体内和个体间睡眠效率均与较低的餐后血糖水平显著相关（均 p<0.03）。发现较晚的睡眠中点（午夜时间偏差）与个体间和个体内比较的餐后葡萄糖显著相关（p=0.035 和 p=0.051）。
结论/解释：较差的睡眠效率和较晚的就寝时间与第二天早餐后的餐后血糖反应更为明显相关。个体偏离其正常睡眠模式也与餐后血糖控制较差有关。这些发现强调了睡眠是调节人类代谢健康的一种可改变的非药物治疗靶点。试验注册ClinicalTrials.gov NCT03479866。
