Cited by 1,136Pancreatic function and diabetesDiabetes and associated disordersDiabetes Treatment and Management

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Conversion of adult pancreatic α-cells to β-cells after extreme β-cell loss

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Thorel, Fabrizio, Népote, Virginie, Avril, Isabelle, Kohno, Kenji, Desgraz, Renaud, Chera, Simona, Herrera, Pedro L.·2010·Nature

DOI 10.1038/nature08894PMC PMC2877635

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Abstract

Pancreatic insulin-producing beta-cells have a long lifespan, such that in healthy conditions they replicate little during a lifetime. Nevertheless, they show increased self-duplication after increased metabolic demand or after injury (that is, beta-cell loss). It is not known whether adult mammals can differentiate (regenerate) new beta-cells after extreme, total beta-cell loss, as in diabetes. This would indicate differentiation from precursors or another heterologous (non-beta-cell) source. Here we show beta-cell regeneration in a transgenic model of diphtheria-toxin-induced acute selective near-total beta-cell ablation. If given insulin, the mice survived and showed beta-cell mass augmentation with time. Lineage-tracing to label the glucagon-producing alpha-cells before beta-cell ablation tracked large fractions of regenerated beta-cells as deriving from alpha-cells, revealing a previously disregarded degree of pancreatic cell plasticity. Such inter-endocrine spontaneous adult cell conversion could be harnessed towards methods of producing beta-cells for diabetes therapies, either in differentiation settings in vitro or in induced regeneration.

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Authors: Thorel, F., Népote, V., Avril, I., Kohno, K., Desgraz, R., Chera, S., & Herrera, P. L.
Affiliations: University of Geneva (CH)
Nara Institute of Science and Technology (JP)
Corresponding author: Herrera, Pedro L.
ORCID: Kohno, Kenji
Chera, Simona
Herrera, Pedro L.
Venue: Nature
Publisher: Springer Science and Business Media LLC
Published: 2010-04-04
Volume: 464
Issue: 7292
Pages: 1149-1154
ISSN: 0028-0836 (ISSN-L)
1476-4687
DOI: 10.1038/nature08894
PMC: PMC2877635
OpenAlex: W2323566388
Cited by: 1,136
References: 53
Citations by year: 2026: 27 · 2025: 40 · 2024: 53 · 2023: 45 · 2022: 53 · 2021: 72 · 2020: 82 · 2019: 81 · 2018: 78 · 2017: 74 · 2016: 78 · 2015: 76 · 2014: 78 · 2013: 107 · 2012: 73
FWCI: 100.01
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Licence: www.springer.com/tdm (tdm)
www.springer.com/tdm (vor)
Locations: Nature (publishedVersion)
PubMed (publishedVersion)
PubMed Central (acceptedVersion)
RePEc: Research Papers in Economics (submittedVersion)
Archive ouverte UNIGE (University of Geneva) (submittedVersion, cc-by)
Archive ouverte UNIGE (University of Geneva) (submittedVersion)
Funders: National Institute of Diabetes and Digestive and Kidney Diseases (U01DK072522)
Topics: Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Pancreatic function and diabetes
Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Diabetes and associated disorders
Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Treatment and Management
Keywords: pancreatic beta-cell regeneration, beta-cell ablation, diphtheria toxin, insulin therapy, lineage tracing, diabetes treatment, transgenic mouse model, endocrine differentiation
MeSH terms: Insulin Secretion, Animals, Cell Count, Cell Differentiation, Diphtheria Toxin, Female, Glucagon, Humans, Insulin, Male, Mice, Transgenic, Regeneration, Biomarkers, Cell Death, Cell Lineage, Cell Proliferation, Glucagon-Secreting Cells, Insulin-Secreting Cells, Mice, Rats, Cell Transdifferentiation, Cellular Reprogramming

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Conversion of adult pancreatic α-cells to β-cells after extreme β-cell loss

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