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Mol Metab. 2014 Jan 22;3(3):268-74. doi: 10.1016/j.molmet.2014.01.010. eCollection 2014.

Islet cell plasticity and regeneration.

Author information

1
Institute of Stem Cell Research, Helmholtz Zentrum München, Ingolstädter Landstr. 1, D-85764 Neuherberg, Germany ; Institute of Diabetes and Regeneration Research, Helmholtz Zentrum München, Am Parkring 11, D-85748, Business Campus Garching, Germany.
2
Institute of Stem Cell Research, Helmholtz Zentrum München, Ingolstädter Landstr. 1, D-85764 Neuherberg, Germany ; Institute of Diabetes and Regeneration Research, Helmholtz Zentrum München, Am Parkring 11, D-85748, Business Campus Garching, Germany ; Research Unit of Molecular Epidemiology Institute of Epidemiology II, Helmholtz Zentrum München, Ingolstädter Landstr. 1, D-85764 Neuherberg, Germany.
3
Institute of Stem Cell Research, Helmholtz Zentrum München, Ingolstädter Landstr. 1, D-85764 Neuherberg, Germany ; Institute of Diabetes and Regeneration Research, Helmholtz Zentrum München, Am Parkring 11, D-85748, Business Campus Garching, Germany ; German Center for Diabetes Research (DZD), Germany.

Abstract

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.

KEYWORDS:

Diabetes; Islet architecture; Pancreas plasticity; β-cell neogenesis; β-cell proliferation; β-cell regeneration

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