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The pancreatic islets comprising only 1%-2% of the volume are highly vascularized and innervated mini-organs. They contain five endocrine cell types, including β cells that secrete insulin, which is synthesized as a single polypeptide chain, preproinsulin, processed to proinsulin, and finally to insulin and C-peptide. This process is complex and regulated, involving the Golgi complex, the endoplasmic reticulum, and the secretory granules of the β cell.
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The ability of induced pluripotent stem cells or iPSCs to differentiate into most body cell types has stimulated repair and regenerative medicine research over the past few decades. iPSC-derived blood cells, hepatocytes, beta islet cells, cardiomyocytes, neurons, and other cell types can repair injuries or regenerate damaged tissue in diseases such as diabetes and neurodegenerative disorders.
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Embryonic and induced pluripotent stem cells are excellent models for disease research because of their ability to self-renew and differentiate into most cell types. Somatic cells from a patient are isolated and reprogrammed into induced pluripotent stem cells or iPSCs. These iPSCs are later differentiated into the desired cell type, which mirrors the diseased cell of the patient. In this way, disease models have been created for investigating diseases such as Down syndrome, type I diabetes,...
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The endoplasmic reticulum (ER) of pancreatic β-cells synthesizes preproinsulin, which consists of a signal peptide, A and B chains, and a C-peptide. Preproinsulin is then cleaved and folded into proinsulin, which translocates to the Golgi apparatus for sorting and packaging into secretory granules. In these granules, enzymatic clipping generates insulin and C-peptide.
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Differentiation of Human Pluripotent Stem Cells into Insulin-Producing Islet Clusters
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Pancreatic islet cell plasticity: Pathogenic or therapeutically exploitable?

Neil Tanday1,2, Andrei I Tarasov1, R Charlotte Moffett1

  • 1Diabetes Research Centre, School of Biomedical Sciences, Ulster University, Coleraine, Northern Ireland.

Diabetes, Obesity & Metabolism
|October 16, 2023
PubMed
Summary
This summary is machine-generated.

Pancreatic islet cells can change their identity under stress, a process linked to diabetes. Therapies targeting this plasticity may help prevent beta-cell loss and manage diabetes.

Keywords:
diabetesendocrinogenesispancreatic isletstransdifferentiation

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Area of Science:

  • Endocrinology
  • Cell Biology
  • Metabolic Diseases

Background:

  • Pancreatic islet endocrine cell development is a regulated process involving transcription factors essential for mature cell phenotype.
  • Metabolic stress, seen in diabetes, obesity, and pregnancy, can alter beta-cell transcription factors, leading to dedifferentiation or transdifferentiation.
  • This loss of beta-cell identity is implicated in the pathogenesis of diabetes.

Purpose of the Study:

  • To review islet cell plasticity in experimental settings.
  • To discuss the physiological and therapeutic aspects of islet cell plasticity.
  • To focus on strategies for preventing beta-cell loss and generating new beta-cells in diabetes.

Main Methods:

  • Review of existing literature on islet cell plasticity.
  • Analysis of experimental settings demonstrating cell plasticity.
  • Discussion of therapeutic agents and their effects on beta-cell dedifferentiation and transdifferentiation.

Main Results:

  • Antidiabetic agents, including GLP-1 mimetics and novel peptides, can prevent or reverse beta-cell dedifferentiation.
  • These agents may also promote the transdifferentiation of non-beta-cells into insulin-positive beta-cell-like cells.
  • Islet cell plasticity manifests in various experimental models.

Conclusions:

  • Understanding islet cell plasticity is crucial for developing targeted therapies for diabetes.
  • Strategies aimed at preserving beta-cell identity or generating new beta-cells hold therapeutic potential.
  • Further research into the molecular mechanisms of islet cell plasticity is needed to combat beta-cell decline in diabetes.