Late dinner impairs glucose tolerance in MTNR1B risk allele carriers: A randomized, cross-over study
Open accessAbstract
Background & aims Late-night dinner eating is associated with increased risk for type-2 diabetes. The underlying mechanism is unclear. One explanatory hypothesis is that the concurrence of elevated circulating melatonin and high glucose concentrations (characterizing late eating) leads to impaired glucose tolerance. However, to date no study has tested the influence of physiological melatonin concentrations on glucose-tolerance. The discovery of melatonin receptor MTNR1B as a diabetes risk gene provides evidence for a role of physiological levels of melatonin in glucose control. The aim of our study was to test the hypothesis that elevated endogenous melatonin concentrations worsen glucose control when eating late. Registered under ClinicalTrials.gov Identifier no. NCT03003936.Methods We performed a randomized, cross-over trial to compare glucose tolerance in the presence (late dinner) or absence (early dinner) of elevated physiological melatonin concentrations and we compared the results between homozygous carriers and non-carriers of the MTNR1B risk allele.Results The concurrence of meal timing with elevated endogenous melatonin concentrations resulted in impaired glucose tolerance. This effect was stronger in MTNR1B risk-carriers than in non-carriers. Furthermore, eating late significantly impaired glucose tolerance only in risk-carriers and not in the non-risk carriers.Conclusions The interaction of dinner timing with MTNR1B supports a causal role of endogenous melatonin in the impairment of glucose tolerance. These results suggest that moving the dinner to an earlier time may result in better glucose tolerance specially in MTNR1B carriers.Clinical trial registration https://clinicaltrials.gov/ct2/show/NCT03003936.
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A late dinner could be understood as a dinner taken within roughly 2.5 h before bedtime.
“Therefore, a late dinner could be understood as a dinner taken within roughly 2.5 h before bedtime (10).”
From Interplay of Dinner Timing and <i>MTNR1B</i> Type 2 Diabetes Risk Variant on Glucose Tolerance and Insulin Secretion: A Randomized Crossover Trial (2022) · cites this paper as [10]
The Methods (Experimental Design) define the study’s late-dinner condition as dinner one hour before usual bedtime, versus four hours for early dinner. The Discussion recommends dinner no later than 2–4 hours before habitual sleep, but does not establish roughly 2.5 hours as a cutoff for what counts as a late dinner. (LLM, conf=0.83)
Experimental — accuracy not yet measuredThe impairment of glucose tolerance and decrease in insulin secretion during late dinner timing might be partly due to the 3.5-fold higher melatonin concentrations.
“This difference might be partly due to the 3.5-fold higher melatonin concentrations, as supported by our earlier trial in which acute melatonin administration impaired glucose tolerance and in vitro b-cell experiments showing decreased insulin secretion due to melatonin (10,11,18,28).”
From Interplay of Dinner Timing and <i>MTNR1B</i> Type 2 Diabetes Risk Variant on Glucose Tolerance and Insulin Secretion: A Randomized Crossover Trial (2022) · cites this paper as [10]
The Discussion reports that late dinner impaired glucose tolerance in MTNR1B risk carriers and implicates elevated melatonin; the Methods also state that melatonin levels were higher with late dinner. Our copy does not establish the claimed 3.5-fold difference or report decreased insulin secretion in this trial, which measured glucose and salivary melatonin. (LLM, conf=0.85)
Experimental — accuracy not yet measuredThe mechanisms underlying the association between melatonin administration and glycemic control remain unclear.
“While a few other studies (9–14) have examined the effects of melatonin administration on glycemic control, the mechanisms underlying such association remain unclear (7).”
From Melatonin Impairs Glucose Tolerance, First-Phase Insulin Secretion, and Insulin Feedback Inhibition; Interaction With <i>MTNR1B</i> Diabetes Risk Variant (2026) · cites this paper as [13]
The Introduction says the cause of reduced glucose tolerance with night eating is unknown and reports that administered melatonin impairs glucose tolerance. The Discussion offers a potential receptor-mediated mechanism, but the paper does not specifically state that the mechanisms linking melatonin administration to glycemic control remain unclear; its explicit uncertainty concerns night eating and physiological melatonin levels. (LLM, conf=0.78)
Experimental — accuracy not yet measuredThe risk allele within melatonin receptor MTNR1B provides a link between late dinner eating and impaired glucose tolerance, whereas in non-risk carriers this relation was less pronounced.
“the risk allele within melatonin receptor MTNR1B provides a link between late dinner eating and impaired glucose tolerance, whereas in non-risk carriers, this relation was less pronounced (149).”
From Meal timing and its role in obesity and associated diseases (2024) · cites this paper as [149]
High endogenous levels of melatonin contribute to the impairment of glucose tolerance during the biological night.
“We and others have proposed that high endogenous levels of melatonin contribute to the impairment of glucose tolerance during the biological night (10).”
From Interplay of Dinner Timing and <i>MTNR1B</i> Type 2 Diabetes Risk Variant on Glucose Tolerance and Insulin Secretion: A Randomized Crossover Trial (2022) · cites this paper as [10]
Pilot data in 40 habitual late eaters demonstrated that the concurrence of food intake with elevated endogenous melatonin concentrations can result in impaired glucose tolerance, particularly among carriers of the G risk allele at MTNR1B.
“Our pilot data investigating dinner timing in 40 habitual late eaters (those who self-reported dinner within 2.5 h of their bedtime) demonstrated that the concurrence of food intake with elevated endogenous melatonin concentrations can result in impaired glucose tolerance, particularly among carriers of the G risk allele at this locus (10); however, the physiological mechanism underlying these find”
From Interplay of Dinner Timing and <i>MTNR1B</i> Type 2 Diabetes Risk Variant on Glucose Tolerance and Insulin Secretion: A Randomized Crossover Trial (2022) · cites this paper as [10]
In a pilot study with identical mixed meals under EE and LE dinner conditions, similar effects were observed.
“However, we observed similar effects when mixed meals were given instead of an OGTT (10).”
From Interplay of Dinner Timing and <i>MTNR1B</i> Type 2 Diabetes Risk Variant on Glucose Tolerance and Insulin Secretion: A Randomized Crossover Trial (2022) · cites this paper as [10]
Earlier work shows that elevated melatonin-whether from exogenous administration or due to the endogenous evening rise-acutely impairs glucose tolerance, with stronger effects in MTNR1B risk allele carriers.
“The present results align with and extend our earlier work showing that elevated melatonin—whether from exogenous administration or due to the endogenous evening rise—acutely impairs glucose tolerance, with stronger effects in MTNR1B risk allele carriers (11–14).”
From Melatonin Impairs Glucose Tolerance, First-Phase Insulin Secretion, and Insulin Feedback Inhibition; Interaction With <i>MTNR1B</i> Diabetes Risk Variant (2026) · cites this paper as [13]
Moving the evening dinner to an earlier time may improve glucose tolerance due to a causal role of endogenous melatonin in the impairment of glucose tolerance, particularly in MTNR1B carriers.
“It has also been shown that moving the evening dinner to an earlier time may improve glucose tolerance due to a causal role of endogenous melatonin in the impairment of glucose tolerance, particularly in MTNR18 carriers [310].”
From Effects of diet, lifestyle, Chrononutrition and alternative dietary interventions on postprandial Glycemia and insulin resistance (2022) · cites this paper as [310]
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- Authors
- Lopez-Minguez, J., Saxena, R., Bandín, C., Scheer, F. A., & Garaulet, M.
- Affiliations
- Broad Institute (US)
- Instituto Murciano de Investigación Biosanitaria (ES)
- Brigham and Women's Hospital (US)
- Corresponding author
- Scheer, Frank A.
- Garaulet, Marta
- Venue
- Clinical Nutrition
- Publisher
- Elsevier BV
- Published
- 2018-08
- Volume
- 37
- Issue
- 4
- Pages
- 1133-1140
- ISSN
- 0261-5614 (ISSN-L)
- PMC
- PMC5634913
- OpenAlex
- W2605902884
- Cited by
- 124
- References
- 40
- Citations by year
- 2026: 12 · 2025: 10 · 2024: 19 · 2023: 14 · 2022: 23 · 2021: 20 · 2020: 15 · 2019: 5 · 2018: 6
- FWCI
- 4.36
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Clinical Nutrition (acceptedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Ministerio de Economía y Competitividad
- European Regional Development Fund
- National Institutes of Health (R01 DK102696, R01 HL118601, R01 DK099512, R01 DK105072)
- Topics
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Circadian rhythm and melatonin
- Health Sciences › Medicine › Physiology › Dietary Effects on Health
- Social Sciences › Psychology › Experimental and Cognitive Psychology › Sleep and related disorders
- Keywords
- late dinner, meal timing, glucose tolerance, melatonin, MTNR1B, melatonin receptors, type 2 diabetes risk, endogenous melatonin
- MeSH terms
- Adult, Blood Glucose, Female, Glucose Tolerance Test, Humans, Melatonin, Middle Aged, Obesity, Sleep, Time Factors, Cross-Over Studies, Polymorphism, Single Nucleotide, Receptor, Melatonin, MT2, Meals
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