Melatonin receptors in pancreatic islets: good morning to a novel type 2 diabetes gene
Open accessAbstract
Melatonin is a circulating hormone that is primarily released from the pineal gland. It is best known as a regulator of seasonal and circadian rhythms; its levels are high during the night and low during the day. Interestingly, insulin levels also exhibit a nocturnal drop, which has previously been suggested to be controlled, at least in part, by melatonin. This regulation can be explained by the proposed inhibitory action of melatonin on insulin release. Indeed, both melatonin receptor 1A (MTNR1A) and MTNR1B are expressed in pancreatic islets. The role of melatonin in the regulation of glucose homeostasis has been highlighted by three independent publications based on genome-wide association studies of traits connected with type 2 diabetes, such as elevated fasting glucose, and, subsequently, of the disease itself. The studies demonstrate a link between variations in the MTNR1B gene, hyperglycaemia, impaired early phase insulin secretion and beta cell function. The risk genotype predicts the future development of type 2 diabetes. Carriers of the risk genotype exhibit increased expression of MTNR1B in islets. This suggests that these individuals may be more sensitive to the actions of melatonin, leading to impaired insulin secretion. Blocking the inhibition of insulin secretion by melatonin may be a novel therapeutic avenue for type 2 diabetes.
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There exist conflicting data regarding the effects of melatonin and MTNR1B genotype on glucose control and disagreement on whether melatonin increases or decreases fasting glucose, glucose tolerance, and T2D risk.
“There exist conflicting data regarding the effects of melatonin and MTNR1B genotype on glucose control (12)(13)(14) and disagreement on whether melatonin increases or decreases fasting glucose, glucose tolerance, and T2D risk.”
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 [13]
The 'Altering melatonin action in vivo' section (page unavailable) describes contradictory results from studies manipulating melatonin, supporting the claim that its metabolic effects are debated. But the 'Genome-wide association studies and MTNR1B' section says the reported MTNR1B associations consistently point toward elevated fasting glucose and increased type 2 diabetes risk; it does not describe disagreement about their direction or about glucose tolerance. (LLM, conf=0.86)
Experimental — accuracy not yet measuredAn inhibitory effect of melatonin on glucose-stimulated insulin secretion has been reported in isolated rat pancreatic islets and a rat insulinoma cell line.
“Locally, an inhibitory effect of melatonin on glucose-stimulated insulin secretion has been reported in isolated rat pancreatic islets and a rat insulinoma cell line (24,25).”
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 [25]
In “Melatonin and insulin secretion” (page unavailable), the paper reports that melatonin attenuates glucose-stimulated insulin secretion from isolated rat islets and that inhibitory effects have been replicated in clonal beta cells. It also describes impaired insulin secretion in INS-1 cells after melatonin treatment, but does not specify that the INS-1 result was measured under glucose stimulation. (LLM, conf=0.84)
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- Authors
- Mulder, H., Nagorny, C. L. F., Lyssenko, V., & Groop, L.
- Affiliations
- Lund University (SE)
- Corresponding author
- Mulder, H.
- Venue
- Diabetologia
- Published
- 2009-04-18
- Volume
- 52
- Issue
- 7
- Pages
- 1240-1249
- ISSN
- 0012-186X (ISSN-L)
- 1432-0428
- OpenAlex
- W1985401769
- Cited by
- 169
- References
- 69
- Citations by year
- 2026: 5 · 2025: 10 · 2024: 3 · 2023: 4 · 2022: 11 · 2021: 6 · 2020: 7 · 2019: 8 · 2018: 4 · 2017: 8 · 2016: 14 · 2015: 6 · 2014: 15 · 2013: 11 · 2012: 17
- FWCI
- 3.03
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Diabetologia (publishedVersion)
- PubMed (publishedVersion)
- Lund University Publications (Lund University) (submittedVersion)
- Funders
- Eli Lilly and Company
- Sanofi
- European Foundation for the Study of Diabetes
- Lunds Universitet
- Vetenskapsrådet
- Topics
- Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Circadian rhythm and melatonin
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Diabetes and associated disorders
- Keywords
- melatonin receptors, MTNR1A, MTNR1B, pancreatic islets, type 2 diabetes, insulin secretion, glucose homeostasis, circadian rhythm, beta-cell function, risk genotype, hyperglycemia, melatonin
- MeSH terms
- Blood Glucose, Diabetes Mellitus, Type 2, Humans, Risk Factors, Receptors, Melatonin, Genome-Wide Association Study
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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