PUBLICATION

Reinforcing one-carbon metabolism via folic acid/Folr1 promotes β-cell differentiation

Authors
Karampelias, C., Rezanejad, H., Rosko, M., Duan, L., Lu, J., Pazzagli, L., Bertolino, P., Cesta, C.E., Liu, X., Korbutt, G.S., Andersson, O.
ID
ZDB-PUB-210609-3
Date
2021
Source
Nature communications   12: 3362 (Journal)
Registered Authors
Keywords
none
MeSH Terms
  • Animals
  • Animals, Genetically Modified
  • Animals, Newborn
  • Carbon/metabolism*
  • Carnitine/metabolism
  • Cell Differentiation/drug effects*
  • Cell Differentiation/genetics
  • Cells, Cultured
  • Folate Receptor 1/genetics
  • Folate Receptor 1/metabolism*
  • Gene Expression Regulation/drug effects
  • Humans
  • Insulin-Secreting Cells/cytology
  • Insulin-Secreting Cells/metabolism*
  • Larva/genetics
  • Larva/metabolism
  • Leucovorin/pharmacology*
  • Metabolic Networks and Pathways/drug effects
  • Mice
  • Pyrimidines/metabolism
  • Swine
  • Zebrafish/genetics
  • Zebrafish/metabolism*
PubMed
34099692 Full text @ Nat. Commun.
Abstract
Diabetes can be caused by an insufficiency in β-cell mass. Here, we performed a genetic screen in a zebrafish model of β-cell loss to identify pathways promoting β-cell regeneration. We found that both folate receptor 1 (folr1) overexpression and treatment with folinic acid, stimulated β-cell differentiation in zebrafish. Treatment with folinic acid also stimulated β-cell differentiation in cultures of neonatal pig islets, showing that the effect could be translated to a mammalian system. In both zebrafish and neonatal pig islets, the increased β-cell differentiation originated from ductal cells. Mechanistically, comparative metabolomic analysis of zebrafish with/without β-cell ablation and with/without folinic acid treatment indicated β-cell regeneration could be attributed to changes in the pyrimidine, carnitine, and serine pathways. Overall, our results suggest evolutionarily conserved and previously unknown roles for folic acid and one-carbon metabolism in the generation of β-cells.
Genes / Markers
Figures
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Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping