Rare MTNR1B variants impairing melatonin receptor 1B function contribute to type 2 diabetes
Open accessAbstract
Genome-wide association studies have revealed that common noncoding variants in MTNR1B (encoding melatonin receptor 1B, also known as MT(2)) increase type 2 diabetes (T2D) risk(1,2). Although the strongest association signal was highly significant (P < 1 × 10(-20)), its contribution to T2D risk was modest (odds ratio (OR) of ∼1.10-1.15)(1-3). We performed large-scale exon resequencing in 7,632 Europeans, including 2,186 individuals with T2D, and identified 40 nonsynonymous variants, including 36 very rare variants (minor allele frequency (MAF) <0.1%), associated with T2D (OR = 3.31, 95% confidence interval (CI) = 1.78-6.18; P = 1.64 × 10(-4)). A four-tiered functional investigation of all 40 mutants revealed that 14 were non-functional and rare (MAF < 1%), and 4 were very rare with complete loss of melatonin binding and signaling capabilities. Among the very rare variants, the partial- or total-loss-of-function variants but not the neutral ones contributed to T2D (OR = 5.67, CI = 2.17-14.82; P = 4.09 × 10(-4)). Genotyping the four complete loss-of-function variants in 11,854 additional individuals revealed their association with T2D risk (8,153 individuals with T2D and 10,100 controls; OR = 3.88, CI = 1.49-10.07; P = 5.37 × 10(-3)). This study establishes a firm functional link between MTNR1B and T2D risk.
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Enhanced melatonin signaling in MTNR1B G risk allele carriers becomes detrimental for glucose homeostasis.
“(in this case, enhanced melatonin signaling in MTNR1B G risk allele carriers becomes detrimental for glucose homeostasis) (29,30).”
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 [29]
The discussion passage in our copy (labeled Abstract; no page number provided) argues against the proposed mechanism: it says increased MTNR1B expression may not be causal and links impaired MT2 signaling to type 2 diabetes risk. It even suggests melatonin receptor agonists may be beneficial, contrary to the claim that enhanced signaling is detrimental. (LLM, conf=0.88)
Checked by a reasoning model — may be wrong.
Experimental — accuracy not yet measuredThe equilibrium hypothesis states that either exaggerated or dampened melatonin signaling in common and rare variant carriers, respectively, becomes detrimental for glucose homeostasis.
“These results are also in concordance with previous studies that support the”
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 [29]
The paper supports the rare-variant half: its Abstract reports that variants impairing melatonin signaling are associated with type 2 diabetes. But its discussion of the common risk allele says the observed increase in MTNR1B expression is not causal and may instead reflect impaired receptor signaling. That contradicts the claim that exaggerated signaling in common-variant carriers is detrimental. (LLM, conf=0.86)
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- Authors
- The Meta-Analysis of Glucose and Insulin-Related Traits Consortium (MAGIC), Bonnefond, A., Clément, N., Fawcett, K., Yengo, L., Vaillant, E., Guillaume, J.-L., Dechaume, A., Payne, F., Roussel, R., Czernichow, S., Hercberg, S., Hadjadj, S., Balkau, B., Marre, M., Lantieri, O., Langenberg, C., Bouatia-Naji, N., Charpentier, G., Vaxillaire, M., Rocheleau, G., Wareham, N. J., Sladek, R., McCarthy, M. I., Dina, C., Barroso, I., Jockers, R., & Froguel, P.
- Affiliations
- Centre National de la Recherche Scientifique (FR)
- Wellcome Sanger Institute (GB)
- Inserm (FR)
- Université de Versailles Saint-Quentin-en-Yvelines (FR)
- Université Paris-Sud (FR)
- University of Cambridge (GB)
- Centre Hospitalier Sud Francilien (FR)
- Centre Hospitalier de l’Université de Montréal (CA)
- McGill University and Génome Québec Innovation Centre (CA)
- Centre for Human Genetics (GB)
- Corresponding author
- Jockers, Ralf
- Froguel, Philippe
- ORCID
- Bonnefond, Amélie
- Clément, Nathalie
- Fawcett, Katherine
- Yengo, Loïc
- Guillaume, Jean-Luc
- Payne, Felicity
- Roussel, Ronan
- Czernichow, Sébastien
- Hadjadj, Samy
- Balkau, Beverley
- Marre, Michel
- Langenberg, Claudia
- Charpentier, Guillaume
- Vaxillaire, Martine
- Rocheleau, Ghislain
- Wareham, Nicholas J
- Sladek, Robert
- McCarthy, Mark I
- Barroso, Inês
- Jockers, Ralf
- Froguel, Philippe
- Venue
- Nature Genetics
- Published
- 2012-01-29
- Volume
- 44
- Issue
- 3
- Pages
- 297-301
- ISSN
- 1061-4036 (ISSN-L)
- 1546-1718
- PMC
- PMC3773908
- OpenAlex
- W2066199795
- Cited by
- 363
- References
- 32
- Citations by year
- 2026: 3 · 2025: 14 · 2024: 16 · 2023: 12 · 2022: 17 · 2021: 19 · 2020: 26 · 2019: 29 · 2018: 14 · 2017: 27 · 2016: 37 · 2015: 48 · 2014: 46 · 2013: 38 · 2012: 17
- FWCI
- 21.24
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature Genetics (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- HAL (submittedVersion)
- UCL Discovery (University College London) (submittedVersion)
- Site cant be reached (submittedVersion)
- Funders
- Wellcome Trust (077016, 077016/Z/05/Z, 090532)
- Agence Nationale de la Recherche (ANR-10-INBS-0001)
- Topics
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Circadian rhythm and melatonin
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetic Associations and Epidemiology
- Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
- Keywords
- MTNR1B, MT2 receptor, type 2 diabetes, rare variants, loss-of-function mutations, non-synonymous mutations, receptor function, diabetes risk, functional characterization of variants
- MeSH terms
- Amino Acid Sequence, Base Sequence, Diabetes Mellitus, Type 2, Exons, Gene Frequency, Humans, Models, Molecular, Molecular Sequence Data, Genetic Variation, Body Mass Index, Logistic Models, Odds Ratio, Sequence Analysis, DNA, Amino Acid Substitution, Receptor, Melatonin, MT2, White People, Genome-Wide Association Study
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