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 Concept Videos

Inflammatory Bowel Disease III: Crohn's Disease01:25

Inflammatory Bowel Disease III: Crohn's Disease

Crohn’s disease is a chronic, relapsing form of inflammatory bowel disease characterized by segmental, transmural inflammation that can affect any part of the gastrointestinal tract. Its pathogenesis arises from a combination of genetic susceptibility, environmental exposures, epithelial barrier dysfunction, and immune dysregulation. Together, these factors lead to an exaggerated immune response against components of the gut microbiome.Genetic and Environmental InfluencesMultiple genetic...
Inflammatory Bowel Disease II: Ulcerative Colitis01:20

Inflammatory Bowel Disease II: Ulcerative Colitis

Ulcerative colitis is a chronic inflammatory disorder of the colon characterized by continuous mucosal inflammation that typically begins in the rectum and extends proximally in a uniform pattern. Its pathogenesis involves a complex interplay of genetic predisposition, immune dysregulation, and environmental influences. These factors converge to impair the colon’s epithelial defenses and promote an exaggerated inflammatory response against luminal contents.Breakdown of the Mucosal BarrierA...
Inflammatory Bowel Disease I: Introduction01:26

Inflammatory Bowel Disease I: Introduction

Inflammatory bowel disease is a group of chronic disorders marked by recurrent inflammation of the gastrointestinal tract due to an abnormal immune response against gut microflora. This leads to tissue damage. The two main forms are Crohn’s disease and ulcerative colitis.Crohn’s DiseaseCrohn’s disease is a relapsing inflammatory disorder that can affect any part of the GI tract, from the mouth to the anus. It involves all layers of the bowel wall (transmural) and shows “skip lesions” in which...
Inflammatory Bowel Disease III: Diagnostic Studies and Management I-Nutritional Therapy01:30

Inflammatory Bowel Disease III: Diagnostic Studies and Management I-Nutritional Therapy

Various diagnostic tests are employed in the diagnostic process for Inflammatory Bowel Disease (IBD), particularly to differentiate between Crohn's disease and ulcerative colitis.
Diagnostic studies
A colonoscopy is the definitive screening test, distinguishing ulcerative colitis from other colon diseases with similar symptoms. During a colonoscopy test, inflamed mucosa with exudate ulcerations can be observed, and biopsies are taken to determine the histologic characteristics of the colonic...
Inflammatory Bowel Disease II: Crohn's Disease01:30

Inflammatory Bowel Disease II: Crohn's Disease

Introduction
Inflammatory bowel disease, commonly known as IBD, refers to a collection of disorders that lead to persistent inflammation of the gastrointestinal tract. The two types of IBD are ulcerative colitis, which impacts the colon, and Crohn's disease, which can involve any part of the gastrointestinal segment.
Crohn's disease
Crohn's disease is a chronic, systemic inflammatory bowel disease (IBD) that predominantly affects the gastrointestinal tract. It is marked by transmural...
Dysbiosis of the Gut Microbiota01:18

Dysbiosis of the Gut Microbiota

The human gut microbiome includes a diverse array of microbial species, including beneficial commensals and opportunistic pathogens, which interact to support host health. These microbes contribute to essential functions such as nutrient metabolism, immune system modulation, and maintenance of intestinal barrier integrity. However, disruptions to this equilibrium—referred to as dysbiosis—can have widespread physiological consequences.Dysbiosis is often characterized by reduced microbial...

You might also read

Related Articles

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

Sort by
Same author

The ApoA-IV-LRP1 Signaling Axis: A Novel Insulin-Independent Pathway for the Suppression of Diabetic Hyperglucagonemia.

Cells·2026
Same author

Involvement of Periostin in Intestinal Fibrosis Associated With Crohn's Disease.

Journal of gastroenterology and hepatology·2026
Same author

DENND5B disruption results in reduced body fat and increased intestinal fatty acid oxidation by activation of autophagy.

Journal of lipid research·2026
Same author

Prevalence and clinical impact of latent tuberculosis infection in patients with inflammatory bowel disease in Japan: a retrospective multicenter study by the IBD-Quality team.

Journal of gastroenterology·2026
Same author

Efficacy and Recovery of Remimazolam Versus Midazolam in Sedated Colonoscopy: A Multicenter Randomized Controlled Trial in Japan.

Digestive endoscopy : official journal of the Japan Gastroenterological Endoscopy Society·2026
Same author

The Usefulness of Over-the-Scope Clips for Managing Gastrointestinal Complications of Endoscopic or Surgical Procedures: The SAGA-OTSC Registry Study.

JGH open : an open access journal of gastroenterology and hepatology·2025

Related Experiment Video

Updated: Jun 1, 2026

DNBS/TNBS Colitis Models: Providing Insights Into Inflammatory Bowel Disease and Effects of Dietary Fat
09:04

DNBS/TNBS Colitis Models: Providing Insights Into Inflammatory Bowel Disease and Effects of Dietary Fat

Published on: February 27, 2014

Nutrient-induced inflammation in the intestine.

Yong Ji1, Yasuhisa Sakata, Patrick Tso

  • 1Department of Pathology and Laboratory Medicine, Metabolic Diseases Institute, University of Cincinnati, Cincinnati, Ohio 45237, USA.

Current Opinion in Clinical Nutrition and Metabolic Care
|May 19, 2011
PubMed
Summary

Dietary fat absorption triggers intestinal inflammation by activating mast cells and releasing mediators. This process may contribute to inflammatory bowel disease and systemic metabolic syndrome, highlighting far-reaching consequences.

More Related Videos

Induction of Intestinal Inflammation by Adoptive Transfer of CBir1 TCR Transgenic CD4+ T Cells to Immunodeficient Mice
07:34

Induction of Intestinal Inflammation by Adoptive Transfer of CBir1 TCR Transgenic CD4+ T Cells to Immunodeficient Mice

Published on: December 16, 2021

Analyzing Beneficial Effects of Nutritional Supplements on Intestinal Epithelial Barrier Functions During Experimental Colitis
08:58

Analyzing Beneficial Effects of Nutritional Supplements on Intestinal Epithelial Barrier Functions During Experimental Colitis

Published on: January 5, 2017

Related Experiment Videos

Last Updated: Jun 1, 2026

DNBS/TNBS Colitis Models: Providing Insights Into Inflammatory Bowel Disease and Effects of Dietary Fat
09:04

DNBS/TNBS Colitis Models: Providing Insights Into Inflammatory Bowel Disease and Effects of Dietary Fat

Published on: February 27, 2014

Induction of Intestinal Inflammation by Adoptive Transfer of CBir1 TCR Transgenic CD4+ T Cells to Immunodeficient Mice
07:34

Induction of Intestinal Inflammation by Adoptive Transfer of CBir1 TCR Transgenic CD4+ T Cells to Immunodeficient Mice

Published on: December 16, 2021

Analyzing Beneficial Effects of Nutritional Supplements on Intestinal Epithelial Barrier Functions During Experimental Colitis
08:58

Analyzing Beneficial Effects of Nutritional Supplements on Intestinal Epithelial Barrier Functions During Experimental Colitis

Published on: January 5, 2017

Area of Science:

  • Gastroenterology
  • Immunology
  • Nutrition Science

Background:

  • Emerging evidence links nutrient intake to gut inflammation.
  • Dietary factors significantly influence intestinal immune responses.

Purpose of the Study:

  • To review the relationship between nutrient absorption and intestinal inflammation.
  • To highlight the physiological and pathophysiological consequences of fat absorption.

Main Methods:

  • Review of current scientific literature.
  • Analysis of studies using conscious lymph fistula rat models.
  • Examination of clinical data on dietary fat and inflammatory conditions.

Main Results:

  • Fat absorption activates intestinal mucosal mast cells, releasing histamine, rat mucosal mast cell protease II (RMCPII), and prostaglandin D2 (PGD2).
  • Increased animal fat consumption is implicated in inflammatory bowel disease pathogenesis.
  • High-fat diets may contribute to metabolic syndrome and chronic low-grade inflammation.

Conclusions:

  • Understanding nutrient absorption's role in intestinal inflammation is crucial.
  • Further research is needed on the interaction between enterocytes and immune cells in nutrient absorption and gut inflammation.