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Modeling Genetic Risk of β-Cell Dysfunction in Human Induced Pluripotent Stem Cells From Patients Carrying the MTNR1B

Tania Singh1, Sebastian Kalamajski2, Joãp P M C M Cunha1

  • 1Unit of Molecular Metabolism, Lund University Diabetes Centre, Lund, Sweden.

Journal of Pineal Research
|September 3, 2025
PubMed
Summary

Disruptions in circadian rhythm are linked to type 2 diabetes (T2D). A specific gene variant (MTNR1B G-allele) increases T2D risk by affecting melatonin receptor 1B, potentially impairing pancreatic beta-cell function.

Keywords:
melatonin receptor 1Bsingle‐nucleotide polymorphismstem cell derived β‐cellsβ‐cell function

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Area of Science:

  • Endocrinology
  • Genetics
  • Stem Cell Biology

Background:

  • Circadian rhythm disruptions and melatonin signaling are implicated in type 2 diabetes (T2D) pathogenesis.
  • A common variant (rs10830963 G-allele) in the melatonin receptor 1B (MTNR1B) gene is associated with increased T2D risk.
  • This SNP is an expression quantitative trait locus (eQTL) in pancreatic islets, suggesting altered MTNR1B expression impacts beta-cell function.

Purpose of the Study:

  • To investigate the functional impact of the MTNR1B G-allele risk variant on human pancreatic beta-like cells.
  • To elucidate the pathogenic mechanisms linking MTNR1B variants, melatonin signaling, and T2D risk.

Main Methods:

  • Generation of isogenic human induced pluripotent stem cell (hiPSC) and human embryonic stem cell (hESC) lines with either the risk (G/G) or non-risk (C/C) MTNR1B genotype using CRISPR/Cas9.
  • Differentiation of stem cells into beta-like cells over a 50-day protocol.
  • Analysis of MTNR1B protein levels via Western blot and assessment of insulin secretion in response to glucose and melatonin stimulation.

Main Results:

  • Genome editing successfully created isogenic cell lines with >90% accuracy.
  • Western blot analysis showed slightly elevated MTNR1B protein levels in G-allele carrying beta-like cells.
  • While insulin secretion was comparable under glucose stimulation, G-allele cells exhibited increased sensitivity to melatonin's inhibitory effect on insulin secretion.
  • MTNR1B mRNA levels were too low for reliable eQTL analysis in differentiated cells.

Conclusions:

  • Stem cell-derived beta-like cells carrying the MTNR1B risk allele show elevated MTNR1B protein and increased sensitivity to melatonin.
  • These findings suggest a potential functional role for the rs10830963 SNP in MTNR1B-mediated beta-cell dysfunction, contributing to T2D risk.
  • Further validation in more mature beta-cell models is required to confirm these preliminary results.