Background: Although the contribution of the circadian clock to metabolic regulation is widely recognized, the role of meal timing in glucose metabolism and diabetes risk remains insufficiently studied. This study aimed (i) to investigate the link between individual circadian meal timing pattern and glucose homeostasis and (ii) to explore the contribution of genetic and environmental factors to meal timing parameters. Methods: In the German NUtriGenomic Analysis in Twins (NUGAT) cohort, which includes 92 adult twins, glucose metabolism parameters were assessed using fasting samples and the oral glucose tolerance test (OGTT). Parameters of meal timing pattern (meal timing itself, daily calorie distribution, and meal number) were extracted from five-day food records. Circadian eating timing was determined relative to the individual’s chronotype (MSFsc) assessed by the Munich chronotype questionnaire. The heritability of meal timing components was estimated using the ACE model. Results: Multiple meal timing components showed associations with glucose metabolism parameters. Most associations were found for the calorie midpoint defined as the time point at which 50% of daily calories were consumed. Indices of insulin sensitivity, ISI Stumvoll (β = 0.334, p = 2.9 x 10-4) and HOMA-IR (β = -0.276, p = 0.007), as well as fasting insulin levels were significantly associated with the circadian caloric midpoint even after the model adjustment for gender, age, energy intake, and sleep duration. BMI and waist circumference also demonstrated robust associations with circadian caloric midpoint. High or moderate heritability was shown for all meal timing components. Meal timing pattern was also strongly related to individual sleep timing and chronotype, both of which also showed a marked genetic impact. Conclusion: Circadian meal timing is associated with insulin sensitivity and shows significant genetic influences, sharing a common genetic architecture with sleep behaviour. Shifting the main calorie intake to earlier circadian time might protect against diabetes, although this could be challenging due to the high heritability of meal timing components.

The authors have declared no competing interest.

NCT01631123

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 0 315 424 to AFHP).

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Ethics committee of the Charite-Universitaetsmedizin Berlin gave ethical approval for this work

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