Genetic variants in MTNR1B affecting insulin secretion
Open accessAbstract
The incidence of type 2 diabetes mellitus has markedly increased worldwide over the past decades. Pancreatic beta-cell dysfunction as well as central and peripheral insulin resistance appears to be elementary features in the pathophysiology of type 2 diabetes mellitus. Major environmental conditions predisposing to the development of type 2 diabetes are excessive food intake and sedentary life-style on the background of a genetic predisposition. Recent genome-wide association studies identified several novel type 2 diabetes risk genes, with impaired pancreatic beta-cell function as the underlying mechanism of increased diabetes risk in the majority of genes. Many of the novel type 2 diabetes risk genes, including MTNR1B which encodes one of the two known human melatonin receptors, were unexpected at first glance. However, previous animal as well as human studies already pointed to a significant impact of the melatonin system on the regulation of glucose homeostasis, in addition to its well known role in modulation of sleep and circadian rhythms. This brief review aims to give an overview of how alterations in the melatonin system could contribute to an increased diabetes risk, paying special attention to the role of melatonin receptors in pancreatic beta-cell function.
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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 [12]
The section ‘Effects of MTNR1B type 2 diabetes risk variants on β-cell function’ (page not available) describes discrepant findings on melatonin’s effects on insulin secretion and calls some data on melatonin and glucose metabolism controversial. It does not establish disagreement about melatonin’s direction of effect on each of fasting glucose, glucose tolerance, and type 2 diabetes risk; it generally reports MTNR1B risk variants as associated with impaired fasting glucose and increased diabetes risk. (LLM, conf=0.85)
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- Authors
- Müssig, K., Staiger, H., Machicao, F., Häring, H.-U., & Fritsche, A.
- Affiliations
- German Center for Diabetes Research (DE)
- Corresponding author
- Häring, Hans-Ulrich
- Venue
- Annals of Medicine
- Publisher
- Informa UK Limited
- Published
- 2010-07-02
- Volume
- 42
- Issue
- 6
- Pages
- 387-393
- ISSN
- 0785-3890 (ISSN-L)
- 1365-2060
- OpenAlex
- W1971322511
- Cited by
- 38
- References
- 71
- Citations by year
- 2026: 1 · 2025: 2 · 2024: 1 · 2023: 4 · 2022: 3 · 2021: 2 · 2019: 1 · 2018: 5 · 2017: 3 · 2016: 1 · 2015: 3 · 2014: 2 · 2012: 4
- FWCI
- 0.32
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Annals of Medicine (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Circadian rhythm and melatonin
- Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Diabetes and associated disorders
- Keywords
- MTNR1B, melatonin receptors, type 2 diabetes, insulin secretion, beta-cell dysfunction, genetic variants, glucose homeostasis, circadian rhythm, insulin resistance
- MeSH terms
- Insulin Secretion, Animals, Diabetes Mellitus, Type 2, Humans, Insulin, Melatonin, Risk Factors, Genetic Variation, Receptor, Melatonin, MT2, Insulin-Secreting Cells
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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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