MafB Overexpression Enhances Functional Beta Cell Mass

Both Type 1 and Type 2 diabetes are characterized by loss of beta cell function and cell number. Therefore, any cure for diabetes will require increasing a patient's functional beta cell mass. Given that beta cell proliferation is extremely low after adolescence, we have sought to determine gen...

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Bibliographic Details
Published in:The FASEB Journal
Main Authors: Leifer, Aaron H., Tessem, Jeffery Sivert
Format: Article in Journal/Newspaper
Language:English
Published: Wiley 2018
Subjects:
Online Access:http://dx.doi.org/10.1096/fasebj.2018.32.1_supplement.606.2
Description
Summary:Both Type 1 and Type 2 diabetes are characterized by loss of beta cell function and cell number. Therefore, any cure for diabetes will require increasing a patient's functional beta cell mass. Given that beta cell proliferation is extremely low after adolescence, we have sought to determine genetic mechanisms that can result in beta cell proliferation. Recent work has shown that the beta cell transcription factor Nkx6.1, which is essential for beta cell development, is sufficient to enhance glucose‐stimulated insulin secretion, improve beta cell survival and enhance beta cell proliferation. Additional studies have shown similar results for the transcription factor Pdx1. Given these results, we hypothesized that other transcription factors essential for beta cell development may have similar effects on enhancing functional beta cell mass. Here we present data that the transcription factor MafB, which is expressed in early stages of beta cell development, when overexpressed maintains glucose‐stimulated insulin secretion and cell survival, while enhancing beta cell proliferation. These data suggest that MafB may be useful in the process of expanding functional beta cell mass as a treatment for both major forms of diabetes. Support or Funding Information This research was funded by a BYU ORCA Grant to AHL. This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .