Evidence map›Paper›PMID 28303303›Full record

ArticleDiabetologia2017

Melatonin signalling and type 2 diabetes risk: too little, too much or just right?

Hindrik Mulder

Open access · bronzeAbstract readEditorialComment
PubMed Publisher
In one paragraph

Article in Diabetologia, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.2field-weighted citation impact, top 13% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

15 citing papers in PubMed, 32 citations in OpenAlex.

  1. Trial
  2. Nocturnal melatonin secretion and risk of type 2 diabetes: a prospective cohort study.The Journal of clinical endocrinology and metabolism · 2026
    Article
  3. Review
  4. Review
  5. Review
  6. Melatonin Effects on Glucose Metabolism: Time To Unlock the Controversy.Trends in endocrinology and metabolism: TEM · 2020
    Review
  7. Article
  8. Melatonin in type 2 diabetes mellitus and obesity.Nature reviews. Endocrinology · 2019
    Review
  9. Article
  10. Review
  11. Review
  12. Review
  13. Article
  14. Review
  15. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

1 author at 1 institution in 1 country.

Hindrik MulderUnit of Molecular Metabolism, Lund University Diabetes Centre, Jan Waldenströms gata 35, SE-205 02, Malmö, Sweden. hindrik.mulder@med.lu.se.
Lund University · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Of the associations of genetic variants with type 2 diabetes, the one of an SNP in an intron of the gene encoding the melatonin receptor 1B (MTNR1B) has been remarkably robust. Work from our group and others has provided support for a model where carriers of this risk G allele exhibit increased MTNR1B expression in islets of Langerhans. Most published studies to date favour that melatonin's action on the beta cell is inhibition of insulin secretion. Hence, our model proposes that this inhibitory effect of melatonin is exaggerated in carriers of the MTNR1B risk G allele. This would explain why this genetic association causes reduced insulin secretion and greater risk of future type 2 diabetes, as has been observed in numerous studies. Concurrently, another body of work has shown that rare MTNR1B alleles, which could perturb receptor function, also associate with type 2 diabetes. In this commentary, it is suggested that such apparently conflicting observations can be reconciled by the fact that non-coding (intronic; frequent) and coding (exonic; rare) alleles of MTNR1B give rise to different phenotypes. Thus, altered gene transcription may explain why SNPs, which do not alter coding sequences, exhibit cell-specific effects. In contrast, SNPs that change protein sequences are more likely to exert generalised effects since an altered protein will appear in all cells expressing the gene.

Indexed as

AdultDiabetes Mellitus, Type 2FemaleHumansMaleMelatoninMiddle AgedSedentary BehaviorSignal TransductionMelatonincAMPGenome-wide association study (GWAS)G-protein-coupledInhibitory G-protein (Gi)Insulin secretionIsletMelatoninQuantitative trait locusReceptorsSingle nucleotide polymorphism (SNP)

Identifiers

PMID28303303
OpenAlexW2595768508

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.