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Related Concept Videos

Pancreatic Juice and Secretion01:26

Pancreatic Juice and Secretion

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Pancreatic juice is a clear fluid produced by the pancreas, containing water, salts, sodium bicarbonate, and enzymes vital for digestion in the small intestine. It helps break down large molecules, facilitating nutrient absorption.
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Pancreatitis is inflammation of the pancreas, an organ located behind the stomach. It can be either acute or chronic.
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The pancreas, an elongated and flat gland situated behind the stomach, serves a vital function in digesting food and managing blood sugar levels.
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The management of chronic pancreatitis is multifaceted, involving a comprehensive approach that includes thorough assessment, diagnostic testing, and a variety of management strategies.
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Stem cells are undifferentiated cells that divide and produce different types of cells. Ordinarily, cells that have differentiated into a specific cell type are post-mitotic—that is, they no longer divide. However, scientists have found a way to reprogram these mature cells so that they “de-differentiate” and return to an unspecialized, proliferative state. These cells are also pluripotent like embryonic stem cells—able to produce all cell types—and are therefore...
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Acute Pancreatitis II: Clinical Manifestations and Management01:30

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Acute pancreatitis presents a complex medical emergency characterized by rapid onset inflammation of the pancreas, demanding timely diagnosis and management to prevent complications. The condition primarily manifests through severe upper abdominal pain that often radiates to the back. This pain intensifies following the consumption of fatty foods. Accompanying symptoms such as nausea, vomiting, abdominal distention, fever, dyspnea, cyanosis, and jaundice can vary in intensity but significantly...
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Related Experiment Video

Updated: Feb 14, 2026

Differentiation of Human Pluripotent Stem Cells Into Pancreatic Beta-Cell Precursors in a 2D Culture System
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Differentiation of Human Pluripotent Stem Cells Into Pancreatic Beta-Cell Precursors in a 2D Culture System

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Modeling human pancreatic beta cell dedifferentiation.

Marc Diedisheim1, Masaya Oshima1, Olivier Albagli1

  • 1INSERM U1016, Institut Cochin, Université Paris Descartes, 123 Boulevard de Port-Royal, 75014 Paris, France.

Molecular Metabolism
|February 24, 2018
PubMed
Summary

Fibroblast growth factor 2 (FGF2) can cause human pancreatic beta cells to dedifferentiate, a process implicated in type 2 diabetes (T2D). This FGF2-induced dedifferentiation is reversible and linked to increased FGF2 and FGFR1 in T2D patient pancreases.

Keywords:
Beta-cellDedifferentiationHumanType 2 diabetes

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An Efficient Method to Obtain Dedifferentiated Fat Cells
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Area of Science:

  • Cell biology
  • Endocrinology
  • Diabetes research

Background:

  • Reduced functional pancreatic beta-cell mass is a hallmark of type 2 diabetes (T2D).
  • Cellular dedifferentiation is a potential mechanism contributing to this loss of beta-cell function.

Purpose of the Study:

  • To model human beta-cell dedifferentiation using growth factor stimulation.
  • To investigate the role of Fibroblast Growth Factor 2 (FGF2) in beta-cell dedifferentiation.
  • To identify markers of dedifferentiation and explore their relevance in T2D.

Main Methods:

  • Utilized the human beta-cell line EndoC-βH1 and human pancreatic islets.
  • Stimulated cells with Fibroblast Growth Factor 2 (FGF2) to induce dedifferentiation.
  • Analyzed gene expression of beta-cell markers, dedifferentiation markers, and related signaling pathways.
  • Examined transcriptomic data from T2D patient pancreases.

Main Results:

  • FGF2 treatment reduced key beta-cell markers (INS, MAFB, SLC2A2, SLC30A8, GCK) and induced expression of dedifferentiation markers (MYC, HES1, SOX9, NEUROG3).
  • FGF2-induced dedifferentiation was dose-dependent, time-dependent, and reversible upon FGF2 removal.
  • FGF2 treatment upregulated TNFRSF11B, suggesting protection against RANKL signaling.
  • Increased FGF2 expression was observed in non-islet cells of T2D pancreases, alongside elevated FGFR1, SOX9, and HES1 in T2D islets.

Conclusions:

  • Successfully developed an FGF2-induced model for human beta-cell dedifferentiation.
  • Identified novel markers associated with beta-cell dedifferentiation.
  • Provided evidence for increased pancreatic FGF2, FGFR1, and beta-cell dedifferentiation in type 2 diabetes.