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Related Concept Videos

Acute Pancreatitis II: Pathophysiology01:21

Acute Pancreatitis II: Pathophysiology

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The pathophysiology of acute pancreatitis centers on injury to pancreatic acinar cells, which initiates a cascade of harmful intracellular events.This injury leads to premature activation of trypsinogen to trypsin in the pancreas. Trypsin then activates other digestive enzymes, such as chymotrypsin, elastase, and phospholipase A2, which begin breaking down pancreatic tissue. The resulting autodigestion causes local inflammation, tissue swelling, hemorrhage, and fat necrosis.Injured acinar cells...
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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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Cells and Secretions of the Pancreas01:16

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The pancreas, a vital organ within the abdominal cavity, plays dual roles in the digestive and endocrine systems, collaborating with exocrine and endocrine cells to maintain optimal digestion and blood sugar levels.
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Chronic Pancreatitis II: Pathophysiology01:21

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Chronic pancreatitis is a progressive and irreversible inflammation of the pancreas, most often caused by long-term alcohol abuse, but it can also be related to ductal obstruction, smoking, or genetic factors.Chronic pancreatitis occurs when the pancreas is repeatedly exposed to harmful agents like alcohol, smoking, ductal obstruction, or genetic predisposition. These factors lead to the release of toxic metabolites and inflammatory cytokines, sustaining chronic inflammation in the pancreatic...
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After cellular or tissue damage, the resident stem cells present in the human body can locally repair and regenerate the damaged tissue or organ. However, even though some tissues do not have stem cells, they can repair and regenerate with the help of pre-existing cells. For example, beta cells of the pancreas and hepatocytes of the liver can divide to renew and regenerate the tissue. Here, both cell division and cell death are well regulated by homeostasis.
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Chronic stress has been linked to both the onset and progression of serious health conditions, including Type 2 diabetes and cancer. Type 2 diabetes, a widespread chronic illness, is closely associated with obesity and insulin resistance, both of which often worsen under stress. Studies indicate that men experiencing high levels of chronic stress face a 45% higher risk of developing diabetes compared to those with minimal stress. Stress triggers physiological responses that elevate blood...
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Related Experiment Video

Updated: Apr 17, 2026

Isolating and Analyzing Cells of the Pancreas Mesenchyme by Flow Cytometry
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Cellular stress drives pancreatic plasticity.

Ivan A Valdez1, Adrian K K Teo2, Rohit N Kulkarni3

  • 1Section of Islet Cell and Regenerative Biology, Joslin Diabetes Center, Department of Medicine, Brigham and Women's Hospital, and Harvard Medical School, Boston, MA 02215, USA. Department of Cell Biology, Program in Biological and Biomedical Sciences, Graduate School of Arts and Sciences, Harvard University, Cambridge, MA 02138, USA.

Science Translational Medicine
|February 6, 2015
PubMed
Summary

Research explores pancreatic beta cell regeneration, focusing on plasticity for therapeutic applications. Recent studies show potential for converting other cells into insulin-producing cells, offering hope for diabetes treatment.

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Area of Science:

  • Endocrinology
  • Regenerative Medicine
  • Cell Biology

Background:

  • Controversy exists regarding pancreatic beta cell regeneration and the presence of progenitor cells.
  • Previous research has yielded conflicting results on the mechanisms of beta cell replenishment.

Purpose of the Study:

  • To review key findings in pancreatic beta cell regeneration research.
  • To provide a perspective on exploiting pancreatic plasticity for therapeutic beta cell regeneration.

Main Methods:

  • Review of recent studies on pancreatic plasticity.
  • Highlighting examples like in vitro transdifferentiation and in vivo cell conversion.

Main Results:

  • Demonstration of pancreatic exocrine cell transdifferentiation into beta-like cells in vitro.
  • Evidence of in vivo conversion of pancreatic acinar cells to beta-like cells.
  • Potential for redifferentiation of dedifferentiated beta cells in vivo.

Conclusions:

  • Recent advances have renewed interest in pancreatic plasticity for therapeutic purposes.
  • Exploiting human pancreatic plasticity holds promise for future beta cell regeneration therapies.
  • Further research is needed to translate these findings into clinical applications.