Related Experiment Video

Updated: May 13, 2026

Preparing a Mice Model of Severe Acute Pancreatitis via a Combination of Caerulein and Lipopolysaccharide Intraperitoneal Injection
07:38

Preparing a Mice Model of Severe Acute Pancreatitis via a Combination of Caerulein and Lipopolysaccharide Intraperitoneal Injection

Published on: May 10, 2024

GLP-1 based agents and acute pancreatitis : drug safety falls victim to the three monkey paradigm

Edwin A M Gale

    BMJ (Clinical Research Ed.)
    |March 1, 2013
    PubMed
    Abstract

    No abstract available in PubMed .

    More Related Videos

    A Simple and Rapid Method for Simultaneous Isolation of Primary Islets and Primary Pancreatic Acinar Cells from Mice14:39

    A Simple and Rapid Method for Simultaneous Isolation of Primary Islets and Primary Pancreatic Acinar Cells from Mice

    Published on: January 9, 2026

    Sodium Taurocholate Induced Severe Acute Pancreatitis in C57BL/6 Mice06:35

    Sodium Taurocholate Induced Severe Acute Pancreatitis in C57BL/6 Mice

    Published on: June 28, 2021

    Related Concept Videos

    Glucagon-like Receptor Agonists01:24

    Glucagon-like Receptor Agonists

    Incretins include glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP), which stimulate insulin secretion post-meals. In type 2 diabetes, GIP's efficacy is reduced, making GLP-1 a viable drug target. GIP originates from preproGIP.
    GLP-1, when administered in high doses intravenously, triggers insulin secretion, inhibits glucagon release, slows gastric emptying, reduces food intake, and restores normal insulin secretion. However, its rapid inactivation by the...
    Dipeptidyl Peptidase 4 Inhibitors01:23

    Dipeptidyl Peptidase 4 Inhibitors

    Dipeptidyl peptidase 4 (DPP-4) is a serine protease widely distributed in the body. It's involved in the inactivation of GLP-1 and GIP hormones, which are crucial for insulin regulation. DPP-4 inhibitors, such as sitagliptin (Januvia), saxagliptin (Onglyza), linagliptin (Tradjenta), alogliptin (Nesina), and vildagliptin (Galvus), help increase the proportion of active GLP-1, enhancing insulin secretion. These inhibitors work by competitively binding to DPP-4. This binding causes a significant...
    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...
    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...
    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 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...