Document Type

Article

Publication Date

3-6-2018

JAX Source

Cell Rep 2018 Mar 6; 22(10):2667-2676.

Volume

22

Issue

10

First Page

2667

Last Page

2676

ISSN

2211-1247

PMID

29514095

DOI

https://doi.org/10.1016/j.celrep.2018.02.032

Abstract

Many patients with type 1 diabetes (T1D) have residual β cells producing small amounts of C-peptide long after disease onset but develop an inadequate glucagon response to hypoglycemia following T1D diagnosis. The features of these residual β cells and α cells in the islet endocrine compartment are largely unknown, due to the difficulty of comprehensive investigation. By studying the T1D pancreas and isolated islets, we show that remnant β cells appeared to maintain several aspects of regulated insulin secretion. However, the function of T1D α cells was markedly reduced, and these cells had alterations in transcription factors constituting α and β cell identity. In the native pancreas and after placing the T1D islets into a non-autoimmune, normoglycemic in vivo environment, there was no evidence of α-to-β cell conversion. These results suggest an explanation for the disordered T1D counterregulatory glucagon response to hypoglycemia. Cell Rep 2018 Mar 6; 22(10):2667-2676.

Comments

This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

Download

Share

COinS