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


ABSTRACT: Many patients with type 1 diabetes (T1D) have residual ? 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 ? cells and ? 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 ? cells appeared to maintain several aspects of regulated insulin secretion. However, the function of T1D ? cells was markedly reduced, and these cells had alterations in transcription factors constituting ? and ? 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 ?-to-? cell conversion. These results suggest an explanation for the disordered T1D counterregulatory glucagon response to hypoglycemia.

SUBMITTER: Brissova M 

PROVIDER: S-EPMC6368357 | biostudies-literature | 2018 Mar

REPOSITORIES: biostudies-literature

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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  ...[more]

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