Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Experiment Videos

Why does pancreatic overstimulation cause pancreatitis?

Ashok K Saluja1, Markus M Lerch, Phoebe A Phillips

  • 1Department of Surgery, University of Minnesota, Minneapolis, Minnesota 55455, USA. asaluja@umn.edu

Annual Review of Physiology
|October 25, 2006
PubMed
Summary
This summary is machine-generated.

Related Concept Videos

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Loss of the ER-cargo protein CLN8 increases severity of acute pancreatitis and upregulates ER-stress and ER-phagy.

Molecular biomedicine·2026
Same author

Negative impact of reduced exocrine pancreatic function on sarcopenia risk in the asymptomatic general population.

Frontiers in nutrition·2026
Same author

Genome-wide association and Mendelian randomization analyses link <i>Helicobacter pylori</i> infection to Human Leukocyte Antigen polymorphisms and autoimmune diseases.

medRxiv : the preprint server for health sciences·2026
Same author

Bilophila wadsworthia is linked to basal ganglia atrophy in the general population.

Brain, behavior, and immunity·2026
Same author

NLRP3 Inflammasome Activation-Induced Acute Papillitis as a Trigger of Acute Pancreatitis - A Novel Mechanism of Microlithiasis-Induced Acute Pancreatitis.

United European gastroenterology journal·2026
Same author

SLC6A14-mediated carnitine transmembrane uptake from PPARγ<sup>+</sup> cancer-associated fibroblasts promotes recurrence of pancreatic cancer.

Gut·2026
Same journal

CaMKII in the Heart: From Homeostasis to Pathology.

Annual review of physiology·2026
Same journal

Cerebrospinal Fluid-Mediated Brain Clearance: Insights from Human Studies.

Annual review of physiology·2026
Same journal

The Physiological Challenge of Climate Change for Free-Living Terrestrial Mammals.

Annual review of physiology·2026
Same journal

Light Out of Sight: Signaling Mechanisms for Nonvisual Opsins.

Annual review of physiology·2025
Same journal

From Oil Spills to Air Pollution: The Emergence of Phenanthrene as a Ubiquitous Cardiac Toxicant.

Annual review of physiology·2025
Same journal

The Representation of Nociception and Pain in the Developing Brain.

Annual review of physiology·2025
See all related articles

The most common animal model for pancreatitis uses cholecystokinin (CCK) to induce inflammation. This model mimics human pancreatitis by causing early zymogen activation and acinar cell injury.

Area of Science:

  • Gastroenterology
  • Pathology
  • Animal Models

Background:

  • Pancreatitis is an inflammatory pancreatic disorder with several available animal models.
  • The secretagogue hyperstimulation model is the most frequently utilized for pancreatitis research.

Purpose of the Study:

  • To investigate the pathogenesis of pancreatitis using the secretagogue hyperstimulation model.
  • To understand the early events in secretagogue-induced pancreatitis.

Main Methods:

  • Animals were infused with high doses of cholecystokinin (CCK).
  • Observed outcomes included hyperamylasemia, pancreatic edema, and acinar cell injury.

Main Results:

  • CCK infusion closely mimics human pancreatitis.

Related Experiment Videos

  • Intra-acinar zymogen activation is an early pathogenic event.
  • Lysosomal hydrolases activate digestive zymogens, leading to acinar cell injury and necrosis.
  • Acinar cells release cytokines and chemokines, initiating inflammation and systemic disease phases.

    • Conclusions:

    • The secretagogue hyperstimulation model is effective for studying pancreatitis pathogenesis.
    • Early intra-acinar zymogen activation and subsequent acinar cell injury are critical in pancreatitis development.
    • Acinar cell-derived inflammatory mediators play a key role in initiating the inflammatory cascade.