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Related Concept Videos

Acute Pancreatitis II: Pathophysiology01:21

Acute Pancreatitis II: Pathophysiology

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...
Chronic Pancreatitis II: Pathophysiology01:21

Chronic Pancreatitis II: Pathophysiology

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...
Acute Pancreatitis I: Introduction01:27

Acute Pancreatitis I: Introduction

Pancreatitis is inflammation of the pancreas, an organ located behind the stomach. It can be either acute or chronic.
Acute pancreatitis is characterized by rapid inflammation of the pancreas, often caused by factors like gallstone blockage or excessive alcohol consumption. Chronic pancreatitis, on the other hand, is a slow, progressive inflammation that may result from long-term alcohol abuse, obstructions in the pancreatic duct, or genetic factors.
The causes of acute pancreatitis include:
Acute Pancreatitis I: Introduction01:25

Acute Pancreatitis I: Introduction

Acute pancreatitis is the sudden inflammation of the pancreas caused by the early activation of digestive enzymes, leading to the autodigestion of pancreatic tissue. This results in local inflammation and, in severe cases, systemic complications.EtiologyUnderstanding the underlying causes is crucial, as identifying the etiology guides treatment and anticipates complications. Acute pancreatitis can be triggered by various factors, typically grouped into the following clinical categories.Biliary...
cAMP-dependent Protein Kinase Pathways01:25

cAMP-dependent Protein Kinase Pathways

Cyclic Adenosine Monophosphate (cAMP) is an essential second messenger that activates protein kinase A (PKA) and regulates various biological processes. A single epinephrine molecule binds to GPCR and activates several heterotrimeric G proteins, each stimulating multiple adenylyl cyclase, amplifying the signal, and synthesizing large numbers of cAMP molecules. Small changes in cAMP concentration affect PKA activity. The binding of four cAMP molecules induces a conformational change in PKA,...
Acute Pancreatitis II: Clinical Manifestations and Management01:30

Acute Pancreatitis II: Clinical Manifestations and Management

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: Jul 14, 2026

Establishment of a Mouse Severe Acute Pancreatitis Model using Retrograde Injection of Sodium Taurocholate into the Biliopancreatic Duct
07:10

Establishment of a Mouse Severe Acute Pancreatitis Model using Retrograde Injection of Sodium Taurocholate into the Biliopancreatic Duct

Published on: April 1, 2022

Pancreatic MAP kinase pathways and acetaldehyde.

M Apte1, J McCarroll, R Pirola

  • 1Pancreatic Research Group, South Western Sydney Clinical School, Liverpool Hospital, the Universify of New South Wales, Sydney, Australia.

Novartis Foundation Symposium
|June 27, 2007
PubMed
Summary

Alcohol metabolism in the pancreas generates toxic byproducts like acetaldehyde, leading to cell damage and pancreatitis. Targeting key molecular pathways, such as MAPK, offers potential therapeutic strategies for alcohol-induced pancreatic injury.

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Preparation of Pancreatic Acinar Cells for the Purpose of Calcium Imaging, Cell Injury Measurements, and Adenoviral Infection
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Preparation of Pancreatic Acinar Cells for the Purpose of Calcium Imaging, Cell Injury Measurements, and Adenoviral Infection

Published on: July 5, 2013

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Last Updated: Jul 14, 2026

Establishment of a Mouse Severe Acute Pancreatitis Model using Retrograde Injection of Sodium Taurocholate into the Biliopancreatic Duct
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Establishment of a Mouse Severe Acute Pancreatitis Model using Retrograde Injection of Sodium Taurocholate into the Biliopancreatic Duct

Published on: April 1, 2022

Preparation of Pancreatic Acinar Cells for the Purpose of Calcium Imaging, Cell Injury Measurements, and Adenoviral Infection
10:39

Preparation of Pancreatic Acinar Cells for the Purpose of Calcium Imaging, Cell Injury Measurements, and Adenoviral Infection

Published on: July 5, 2013

Area of Science:

  • Gastroenterology
  • Molecular Biology
  • Toxicology

Background:

  • Alcohol abuse is a primary cause of pancreatitis, manifesting as acute necroinflammation and chronic damage.
  • Alcohol metabolism produces toxic metabolites (acetaldehyde, FAEEs) and oxidant stress, damaging pancreatic acinar cells.
  • Pancreatic stellate cells (PSCs) are key mediators of alcohol-induced pancreatic fibrosis.

Purpose of the Study:

  • To review the molecular mechanisms underlying alcohol-induced pancreatic injury.
  • To highlight the role of signaling pathways, including MAPK, in acinar cell and PSC responses to alcohol.
  • To identify potential therapeutic targets for preventing or reducing alcohol-induced pancreatitis.

Main Methods:

  • Review of existing literature on alcohol metabolism and pancreatic injury.
  • Analysis of molecular signaling pathways involved in acinar cell and PSC activation.
  • Identification of key mediators and cross-talk between signaling pathways.

Main Results:

  • Ethanol metabolites (acetaldehyde, FAEEs) and oxidant stress induce molecular changes in acinar cells, promoting necroinflammation.
  • Activated PSCs mediate alcohol-induced pancreatic fibrosis.
  • The MAPK pathway is critical in regulating alcohol and acetaldehyde effects on acinar cells and PSCs.
  • NF-kappaB, AP-1, PKC, PI3K, and PPARgamma are key signaling molecules involved in alcohol-induced pancreatic injury.

Conclusions:

  • Understanding the molecular signaling pathways provides a basis for therapeutic interventions.
  • Targeting pathways like MAPK, PI3K, and PPARgamma may prevent or reduce alcohol-induced acute and chronic pancreatic damage.