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Abnormalities in proinsulin processing in islets from individuals with longstanding T1D.

Emily K Sims1, Farooq Syed1, Julius Nyalwidhe2

  • 1Department of Pediatrics, Indiana University School of Medicine, Indianapolis, Indiana; Center for Diabetes and Metabolic Diseases, Indiana University School of Medicine, Indianapolis, Indiana.

Translational Research : the Journal of Laboratory and Clinical Medicine
|August 24, 2019
PubMed
Summary

Persistent proinsulin in type 1 diabetes (T1D) is linked to reduced islet processing enzymes. Inflammatory cytokines decrease these enzymes, impacting beta cell function in long-standing T1D.

Keywords:
CPE = carboxypeptidase EER = endoplasmic reticulumIR = infraredLCM = laser capture microdissectionLFQ = label-free quantificationPC1/3 = prohormone convertase 1/3PC2 = prohormone convertase 2T1D = type 1 diabetesUV = ultravioletnPOD = network for pancreatic organ donors with type 1 diabetes

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Area of Science:

  • Endocrinology
  • Diabetes Research
  • Cell Biology

Background:

  • Individuals with long-standing type 1 diabetes (T1D) often show persistent detectable serum proinsulin, even with undetectable C-peptide.
  • The underlying mechanisms of this persistent proinsulin secretion in T1D islets remain incompletely understood.

Purpose of the Study:

  • To investigate the mechanistic causes of persistent proinsulin secretion in type 1 diabetes (T1D) at the pancreatic islet level.
  • To analyze proinsulin and insulin staining, and the expression of key processing enzymes within human T1D islets.

Main Methods:

  • Immunostaining of human pancreatic sections from T1D donors (n=24) for proinsulin and insulin.
  • Mass spectrometry of laser-capture microdissected human islets (n=6) to analyze proinsulin processing enzyme expression.
  • Quantitative real-time PCR to assess proinsulin processing enzyme mRNA levels in human islets (n=10) treated with inflammatory cytokines.

Main Results:

  • T1D islets showed increased proinsulin-enriched, insulin-poor staining compared to controls.
  • Reduced expression of proinsulin processing enzymes, including prohormone convertase 1/3 (PC1/3) and carboxypeptidase E (CPE), was observed in T1D donor islets.
  • Inflammatory cytokine treatment of human islets decreased mRNA expression of PC1/3, PC2, and CPE.

Conclusions:

  • Altered proinsulin processing occurs in long-duration type 1 diabetes (T1D) islets.
  • Reduced beta cell prohormone processing is associated with inflammatory cytokine-induced downregulation of essential processing enzymes.