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α Cell Function and Gene Expression Are Compromised in Type 1 Diabetes.

Brissova M, Haliyur R, Saunders D, Shrestha S, Dai C, Blodgett DM, Bottino R, Campbell-Thompson M, Aramandla R, Poffenberger G, Lindner J, Pan FC, von Herrath MG, Greiner DL, Shultz LD, Sanyoura M, Philipson LH, Atkinson M, Harlan DM, Levy SE, Prasad N, Stein R, Powers AC
Cell Rep. 2018 22 (10): 2667-2676

PMID: 29514095 · PMCID: PMC6368357 · DOI:10.1016/j.celrep.2018.02.032

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.

Copyright © 2018 The Authors. Published by Elsevier Inc. All rights reserved.

MeSH Terms (21)

Adolescent Adult Animals Case-Control Studies Cellular Reprogramming Child Diabetes Mellitus, Type 1 Female Gene Expression Regulation Glucagon Glucagon-Secreting Cells Humans Insulin-Secreting Cells Insulin Secretion Male Mice Middle Aged Phenotype Tissue Donors Transcription Factors Young Adult

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