IMR Press / FBL / Volume 13 / Issue 15 / DOI: 10.2741/3119

Frontiers in Bioscience-Landmark (FBL) is published by IMR Press from Volume 26 Issue 5 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on as a courtesy and upon agreement with Frontiers in Bioscience.

Open Access Article

Pancreatic acinar-to-beta cell transdifferentiation in vitro

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1 Division of Cellular and Molecular Medicine, Department of Physiology and Cell Biology, Kobe University Graduate School of Medicine, 7-5-1 Kusunoki-cho, Chuo-ku, Kobe 650-0017, Japan
2 Department of Experimental Therapeutics, Translational Research Center, Kyoto University Hospital, 54 Shogoinkawahara-cho, Sakyo-ku, Kyoto 606-8507, Japan
3 Division of Diabetes, Metabolism, and Endocrinology, Department of Internal Medicine, Kobe University Graduate School of Medicine, 7-5-1 Kusunoki-cho, Chuo-ku, Kobe 650-0017, Japan

*Author to whom correspondence should be addressed.

Academic Editor: Myung-Shik Lee

Front. Biosci. (Landmark Ed) 2008, 13(15), 5824–5837;
Published: 1 May 2008
(This article belongs to the Special Issue Recent progress in signal transduction of islet beta cells)

Although accumulating evidence indicates that proliferation of pre-existing beta-cells is the major mechanism of the maintenance of postnatal beta-cell mass, new beta-cells can be generated from non-beta-cells under certain conditions in vitro. We have recently shown directly by Cre/loxP-based cell lineage tracing that adult mouse pancreatic acinar cells can be transdifferentiated into insulin-secreting cells in vitro. These newly made cells secrete insulin in response to glucose and other secretagogues, but their secretory capacity is still low compared to that of native beta-cells. To improve the efficiency of generation of insulin-secreting cells from non-beta cells, it is critical to understand the molecular mechanism of such transdifferentiation. Since pancreatic acinar cells are the most abundant cell type in the pancreas, their utilization as a source of surrogate beta-cells is an intriguing approach to cell replacement therapy for type 1 diabetes. This review focuses on current knowledge of the regeneration of pancreatic beta-cells and transdifferentiation of pancreatic acinar-cells into insulin-secreting cells.

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