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Islet cell plasticity and regeneration()

Insulin-dependent diabetes is a complex multifactorial disorder characterized by loss or dysfunction of β-cells resulting in failure of metabolic control. Even though type 1 and 2 diabetes differ in their pathogenesis, restoring β-cell function is the overarching goal for improved therapy of both di...

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Detalles Bibliográficos
Autores principales: Migliorini, Adriana, Bader, Erik, Lickert, Heiko
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Elsevier 2014
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3986629/
https://www.ncbi.nlm.nih.gov/pubmed/24749056
http://dx.doi.org/10.1016/j.molmet.2014.01.010
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author Migliorini, Adriana
Bader, Erik
Lickert, Heiko
author_facet Migliorini, Adriana
Bader, Erik
Lickert, Heiko
author_sort Migliorini, Adriana
collection PubMed
description Insulin-dependent diabetes is a complex multifactorial disorder characterized by loss or dysfunction of β-cells resulting in failure of metabolic control. Even though type 1 and 2 diabetes differ in their pathogenesis, restoring β-cell function is the overarching goal for improved therapy of both diseases. This could be achieved either by cell-replacement therapy or by triggering intrinsic regenerative mechanisms of the pancreas. For type 1 diabetes, a combination of β-cell replacement and immunosuppressive therapy could be a curative treatment, whereas for type 2 diabetes enhancing endogenous mechanisms of β-cell regeneration might optimize blood glucose control. This review will briefly summarize recent efforts to allow β-cell regeneration where the most promising approaches are currently (1) increasing β-cell self-replication or neogenesis from ductal progenitors and (2) conversion of α-cells into β-cells.
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spelling pubmed-39866292014-04-18 Islet cell plasticity and regeneration() Migliorini, Adriana Bader, Erik Lickert, Heiko Mol Metab Review Insulin-dependent diabetes is a complex multifactorial disorder characterized by loss or dysfunction of β-cells resulting in failure of metabolic control. Even though type 1 and 2 diabetes differ in their pathogenesis, restoring β-cell function is the overarching goal for improved therapy of both diseases. This could be achieved either by cell-replacement therapy or by triggering intrinsic regenerative mechanisms of the pancreas. For type 1 diabetes, a combination of β-cell replacement and immunosuppressive therapy could be a curative treatment, whereas for type 2 diabetes enhancing endogenous mechanisms of β-cell regeneration might optimize blood glucose control. This review will briefly summarize recent efforts to allow β-cell regeneration where the most promising approaches are currently (1) increasing β-cell self-replication or neogenesis from ductal progenitors and (2) conversion of α-cells into β-cells. Elsevier 2014-01-22 /pmc/articles/PMC3986629/ /pubmed/24749056 http://dx.doi.org/10.1016/j.molmet.2014.01.010 Text en © 2014 The Authors http://creativecommons.org/licenses/by-nc-nd/3.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution-NonCommercial-No Derivative Works License, which permits non-commercial use, distribution, and reproduction in any medium, provided the original author and source are credited.
spellingShingle Review
Migliorini, Adriana
Bader, Erik
Lickert, Heiko
Islet cell plasticity and regeneration()
title Islet cell plasticity and regeneration()
title_full Islet cell plasticity and regeneration()
title_fullStr Islet cell plasticity and regeneration()
title_full_unstemmed Islet cell plasticity and regeneration()
title_short Islet cell plasticity and regeneration()
title_sort islet cell plasticity and regeneration()
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3986629/
https://www.ncbi.nlm.nih.gov/pubmed/24749056
http://dx.doi.org/10.1016/j.molmet.2014.01.010
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