Janna Vahlhaus, Beeke Peters, Silke Hornemann, Anne-Cathrin Ost, Michael Kruse, Andreas Busjahn, Andreas F H Pfeiffer, Olga Pivovarova-Ramich
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引用次数: 0
Abstract
Background: Although the contribution of the circadian clock to metabolic regulation is widely recognized, the role of eating timing in glucose metabolism and diabetes risk remains insufficiently studied. This study aimed (i) to investigate the link between the eating timing pattern relative to individual clock and glucose homoeostasis and (ii) to explore the contribution of genetic and environmental factors to eating timing parameters.
Methods: In 92 adult twins (NCT01631123), glycaemic traits were assessed using the oral glucose tolerance test. Parameters of eating timing pattern (eating timing itself, daily calorie distribution, and eating frequency) were extracted from five-day food records. Caloric midpoint defined as the time point at which 50% of daily calories are consumed. Circadian timing of eating was determined as a time interval between the clock time of eating and a corrected midpoint of sleep, a chronotype marker. Heritability of eating timing components was estimated by comparing correlations within monozygotic and dizygotic twin pairs and fitting genetic structural equation models.
Findings: Among components of eating timing, the most associations were found for the circadian time of caloric midpoint (CCM). Later CCM was significantly associated with poorer insulin sensitivity, i.e. with lower ISI Stumvoll (β = 0.304, p = 5.9 × 10-4) and higher HOMA-IR (β = -0.258, p = 0.011) indices, as well as with higher fasting insulin levels (β = -0.259, p = 0.013), even after the model adjustment for sex, age, daily energy intake, and sleep duration. Later CCM also demonstrated robust associations with higher BMI and waist circumference. All eating timing components showed high or moderate heritability and were strongly related to individual sleep timing.
Interpretation: Later eating timing in relation to an individual internal clock is associated with lower insulin sensitivity. Shifting the main calorie intake to earlier circadian times may improve glucose metabolism, but genetic factors could influence the feasibility and effectiveness of eating-timing based interventions. The findings should be investigated in a larger cohort.
Funding: This work was supported by the German Research Foundation (DFG RA 3340/4-1 to OP-R, project number 530918029), by the European Association for the Study of Diabetes (Morgagni Prize 2020 to OP-R), and by the German Federal Ministry of Education and Research (BMBF NUGAT 0315424 to AFHP). The DZD is funded by the German Federal Ministry for Education and Research (01GI0925).
背景:虽然生物钟对代谢调节的贡献已被广泛认识,但进食时间在葡萄糖代谢和糖尿病风险中的作用仍未得到充分研究。本研究旨在(1)探讨与个体生物钟相关的进食时间模式与葡萄糖稳态之间的联系;(2)探讨遗传和环境因素对进食时间参数的影响。方法:采用口服糖耐量试验对92例成年双胞胎(NCT01631123)的血糖特征进行评估。进食时间模式的参数(进食时间本身、每日卡路里分布和进食频率)从五天的食物记录中提取。热量中点定义为每天消耗50%热量的时间点。进食的昼夜节律时间被确定为进食的时钟时间和修正的睡眠中点之间的时间间隔,这是一种时间型标记。通过比较同卵双胞胎和异卵双胞胎之间的相关性,并拟合遗传结构方程模型,估计了进食时间成分的遗传力。研究结果:在进食时间的组成部分中,发现与热量中点(CCM)的昼夜节律时间最相关。后来的CCM与较差的胰岛素敏感性显著相关,即较低的ISI Stumvoll (β = 0.304, p = 5.9 × 10-4)和较高的HOMA-IR (β = -0.258, p = 0.011)指数,以及较高的空腹胰岛素水平(β = -0.259, p = 0.013),即使在对性别、年龄、每日能量摄入和睡眠时间进行模型调整后也是如此。后来的CCM也被证明与较高的BMI和腰围有密切的联系。所有饮食时间因素都显示出高或中等的遗传性,并与个体睡眠时间密切相关。解释:较晚的进食时间与个人体内生物钟有关,与较低的胰岛素敏感性有关。将主要卡路里摄入量调整到较早的昼夜节律时间可能会改善葡萄糖代谢,但遗传因素可能会影响进食时间干预的可行性和有效性。这些发现应该在更大的队列中进行调查。资助:这项工作得到了德国研究基金会(DFG RA 3340/4-1 to OP-R,项目编号530918029)、欧洲糖尿病研究协会(2020年摩根尼奖给OP-R)和德国联邦教育和研究部(BMBF nuga0315424 to AFHP)的支持。DZD由德国联邦教育和研究部(01GI0925)资助。
EBioMedicineBiochemistry, Genetics and Molecular Biology-General Biochemistry,Genetics and Molecular Biology
CiteScore
17.70
自引率
0.90%
发文量
579
审稿时长
5 weeks
期刊介绍:
eBioMedicine is a comprehensive biomedical research journal that covers a wide range of studies that are relevant to human health. Our focus is on original research that explores the fundamental factors influencing human health and disease, including the discovery of new therapeutic targets and treatments, the identification of biomarkers and diagnostic tools, and the investigation and modification of disease pathways and mechanisms. We welcome studies from any biomedical discipline that contribute to our understanding of disease and aim to improve human health.