ReviewCurrent diabetes reports2017
Disentangling the Role of Melatonin and its Receptor MTNR1B in Type 2 Diabetes: Still a Long Way to Go?
Review in Current diabetes reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 31 citations in OpenAlex.
- Melatonin MT1 Receptor Expression in Luminal Invasive Ductal Breast Carcinoma in Postmenopausal Women.Biomolecules · 2025Article
- A Bibliometric Study from 1992 to 2023 on the Relationship between Biological Clock and Diabetes.Endocrine, metabolic & immune disorders drug targets · 2025Article
- Defining type 2 diabetes polygenic risk scores through colocalization and network-based clustering of metabolic trait genetic associations.Genome medicine · 2024Article
- Melatonin improved glucose homeostasis is associated with the reprogrammed gut microbiota and reduced fecal levels of short-chain fatty acids in db/db mice.Food science & nutrition · 2023Article
- An early prediction model for gestational diabetes mellitus based on genetic variants and clinical characteristics in China.Diabetology & metabolic syndrome · 2022Article
- Type 2 diabetes is associated with the MTNR1B gene, a genetic bridge between circadian rhythm and glucose metabolism, in a Turkish population.Molecular biology reports · 2021Article
- New Horizons: Circadian Control of Metabolism Offers Novel Insight Into the Cause and Treatment of Metabolic Diseases.The Journal of clinical endocrinology and metabolism · 2021Review
- Article
- Melatonin Relations with Energy Metabolism as Possibly Involved in Fatal Mountain Road Traffic Accidents.International journal of molecular sciences · 2020Review
- Prognostic Impact of Melatonin Receptors MT1 and MT2 in Non-Small Cell Lung Cancer (NSCLC).Cancers · 2019Article
- Melatonin in type 2 diabetes mellitus and obesity.Nature reviews. Endocrinology · 2019Review
- Melatonin: Countering Chaotic Time Cues.Frontiers in endocrinology · 2019Article
- Type 2 diabetes genetic loci informed by multi-trait associations point to disease mechanisms and subtypes: A soft clustering analysis.PLoS medicine · 2018Article
- Review
- Hypertension genomics and cardiovascular prevention.Annals of translational medicine · 2018Review
- Exposure to Night-Time Traffic Noise, Melatonin-Regulating Gene Variants and Change in Glycemia in Adults.International journal of environmental research and public health · 2017Article
- Central Circadian Clock Regulates Energy Metabolism.Advances in experimental medicine and biologyReview
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purpose of reviewType 2 diabetes (T2D) is a complex genetic metabolic disorder. T2D heritability has been estimated around 40-70%. In the last decade, exponential progress has been made in identifying T2D genetic determinants, through genome-wide association studies (GWAS). Among single-nucleotide polymorphisms mostly associated with T2D risk, rs10830963 is located in the MTNR1B gene, encoding one of the two receptors of melatonin, a neurohormone involved in circadian rhythms. Subsequent studies aiming to disentangle the role of MTNR1B in T2D pathophysiology led to controversies. In this review, we will tackle them and will try to give some directions to get a better view of MTNR1B contribution to T2D pathophysiology. RECENT
findingsRecent studies either based on genetic/genomic analyses, clinical/epidemiology data, functional analyses at rs10830963 locus, insulin secretion assays in response to melatonin (involving or not MTNR1B) or animal model analyses have led to strong controversies at each level of interpretation. We discuss possible caveats in these studies and present ways to go beyond these issues, towards a better understanding of T2D molecular mechanisms, keeping in mind that melatonin is a versatile hormone and regulates many functions via its primary role in the body clock.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.