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

Marcela Brissova1, Rachana Haliyur2, Diane Saunders2

  • 1Department of Medicine, Division of Diabetes, Endocrinology and Metabolism, Vanderbilt University Medical Center, Nashville, TN, USA.

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|March 8, 2018
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Summary

Patients with type 1 diabetes (T1D) retain some insulin-producing beta cells but have impaired glucagon responses. This study reveals altered alpha cell function and identity in T1D, explaining the defective counterregulatory glucagon response.

Keywords:
alpha cellsglucagonhumaninsulinpancreatic islettype 1 diabetes

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Area of Science:

  • Endocrinology
  • Cell Biology
  • Diabetes Research

Background:

  • Type 1 diabetes (T1D) is characterized by autoimmune destruction of insulin-producing beta cells.
  • Despite beta cell loss, some patients retain residual C-peptide producing beta cells.
  • The function of alpha cells and their role in T1D pathogenesis, particularly concerning glucagon response to hypoglycemia, remains unclear.

Purpose of the Study:

  • To investigate the characteristics of residual beta cells and alpha cells in the type 1 diabetes islet endocrine compartment.
  • To understand the functional and transcriptional alterations in T1D alpha cells.
  • To determine if alpha-to-beta cell conversion occurs in T1D.

Main Methods:

  • Analysis of human type 1 diabetes pancreas and isolated islets.
  • Assessment of insulin secretion from remnant beta cells.
  • Evaluation of alpha cell function and transcription factor expression.
  • In vivo studies of T1D islets in a non-autoimmune environment.

Main Results:

  • Residual beta cells in T1D maintain some regulated insulin secretion.
  • Alpha cells in T1D exhibit significantly reduced function and altered transcription factors related to cell identity.
  • No evidence of alpha-to-beta cell conversion was observed in the native pancreas or in vivo.

Conclusions:

  • The functional decline and altered identity of alpha cells contribute to the impaired glucagon response in type 1 diabetes.
  • The findings suggest that alpha cell dysfunction, rather than cell conversion, is key to understanding counterregulatory defects in T1D.