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

Pathophysiology of Peptic Ulcer Disease: Injurious Factors01:22

Pathophysiology of Peptic Ulcer Disease: Injurious Factors

Peptic ulcers are sores on the stomach's inner lining and the upper small intestine, which are the result of disruptions in the mucosal layer that houses parietal cells which produce gastric acid, and chief cells which secrete pepsinogen.
In the antrum region, G cells secrete the gastrin hormone that binds to gastrin-cholecystokinin-B (CCK2) receptors on parietal and enterochromaffin-like (ECL) cells in the fundic glands. Simultaneously, the vagus nerve releases acetylcholine, which binds to M3...
Pathophysiology of Peptic Ulcer Disease: Mucosal Defense Factors01:24

Pathophysiology of Peptic Ulcer Disease: Mucosal Defense Factors

Peptic ulcer disease, commonly called PUD, represents a multifaceted condition characterized by disruptions in the lining of the gastrointestinal (GI)  tract. Central to the protection of the gastrointestinal lining is the mucosal-bicarbonate barrier. This physiological defense mechanism is a formidable shield against the corrosive effects of gastric acid and pepsin secretion in the stomach. Its role is pivotal in maintaining the structural integrity of the stomach's inner lining. Bicarbonate,...
Pharmacogenetic Phenotypes: Alterations in Pharmacokinetics, Drug Targets and Biologic Milieu01:29

Pharmacogenetic Phenotypes: Alterations in Pharmacokinetics, Drug Targets and Biologic Milieu

Genetic variations significantly influence drug response through pharmacokinetics, receptor interactions, and biologic milieu modifications. Pharmacokinetic alterations impact drug metabolism and clearance, affecting efficacy and toxicity. Variants in drug-metabolizing enzymes, such as CYP2C9 and CYP2C19, alter drug activation and elimination. For example, CYP2C9 loss-of-function variants require lower warfarin doses to prevent excessive bleeding, while CYP2C19 variants reduce clopidogrel...
Peptic Ulcer Disease I: Introduction01:30

Peptic Ulcer Disease I: Introduction

Peptic Ulcer Disease (PUD) is characterized by mucosal excavation in the esophagus, stomach, pylorus, or duodenum. It can manifest as acute or chronic based on the extent and duration of mucosal involvement.
An acute ulcer, marked by superficial erosion and minimal inflammation, swiftly resolves upon identifying and addressing the underlying cause. In contrast, a chronic ulcer persists, potentially eroding through the muscular wall and forming fibrous tissue.
Peptic ulcers can also be...
Peptic Ulcer Disease I: Introduction01:25

Peptic Ulcer Disease I: Introduction

Peptic ulcer disease (PUD) involves breaks in the gastrointestinal tract's mucosal lining, primarily in the stomach and duodenum, with less frequent occurrences in the lower esophagus or near the pylorus.Ulcers can be acute or chronic. Acute ulcers are short-lived with minimal inflammation and heal quickly after the irritant is removed. Chronic ulcers persist, may recur, and often cause scarring due to ongoing tissue damage. Superficial erosions affect only the mucosal layer and are called...
Pharmacogenomics: Identification of New Drug Targets01:29

Pharmacogenomics: Identification of New Drug Targets

Advances in genomics have profoundly influenced drug discovery by increasing both the speed and accuracy of pharmaceutical development. Pharmacogenomics, which examines how genetic variation influences drug response, facilitates the identification of novel therapeutic targets and enables patient stratification for personalized treatment. These strategies contribute to improved drug efficacy, minimized adverse effects, and more efficient clinical trial design.Mapping genetic differences...

You might also read

Related Articles

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

Sort by
Same author

Magnesium-Rich Mineral Water Improves Stool Consistency and Bowel Habits in Healthy Subjects: A Randomized Controlled Trial.

Neurogastroenterology and motility·2026
Same author

Initial Treatment Failure as a Predictor of Proximal Extension in Patients with Newly Diagnosed Limited Ulcerative Colitis: A Retrospective Cohort Study with Propensity Score-Matched Analysis.

Digestive diseases and sciences·2025
Same author

Long-Term Outcomes After Therapeutic Induction in Patients with Functional Dyspepsia.

Journal of clinical medicine·2025
Same author

Effect of Chronic Social Defeat Stress on the Small-Intestinal Environment, Including the Gut Flora, Immune System, and Mucosal Barrier Integrity.

International journal of molecular sciences·2025
Same author

Endoscopic indigo carmine spraying for evaluation of intestinal mucosal permeability: Prospective pilot study.

Endoscopy international open·2025
Same author

Sympathetic Overactivation Drives Colonic Eosinophil Infiltration Linked to Visceral Hypersensitivity in Irritable Bowel Syndrome.

Cellular and molecular gastroenterology and hepatology·2025

Related Experiment Video

Updated: Jun 3, 2026

Multi-Gene Single Nucleotide Polymorphism Detection in Gastric Cancer Based on Ion Semiconductor Sequencing Platform
06:21

Multi-Gene Single Nucleotide Polymorphism Detection in Gastric Cancer Based on Ion Semiconductor Sequencing Platform

Published on: May 10, 2024

Genetic factors for functional dyspepsia.

Tadayuki Oshima1, Fumihiko Toyoshima, Shigemi Nakajima

  • 1Division of Upper Gastroenterology, Department of Internal Medicine, Hyogo College of Medicine, Nishinomiya, Hyogo, Japan. t-oshima@hyo-med.ac.jp

Journal of Gastroenterology and Hepatology
|March 30, 2011
PubMed
Summary

Genetic factors contribute to functional dyspepsia (FD) susceptibility, but findings on specific gene polymorphisms remain inconsistent across populations. Further research is needed to clarify these genetic links.

More Related Videos

The Dyspepsia Educational Tool As a Novel Aid in Dyspepsia Management
06:40

The Dyspepsia Educational Tool As a Novel Aid in Dyspepsia Management

Published on: June 29, 2019

An Allele-specific Gene Expression Assay to Test the Functional Basis of Genetic Associations
10:17

An Allele-specific Gene Expression Assay to Test the Functional Basis of Genetic Associations

Published on: November 3, 2010

Related Experiment Videos

Last Updated: Jun 3, 2026

Multi-Gene Single Nucleotide Polymorphism Detection in Gastric Cancer Based on Ion Semiconductor Sequencing Platform
06:21

Multi-Gene Single Nucleotide Polymorphism Detection in Gastric Cancer Based on Ion Semiconductor Sequencing Platform

Published on: May 10, 2024

The Dyspepsia Educational Tool As a Novel Aid in Dyspepsia Management
06:40

The Dyspepsia Educational Tool As a Novel Aid in Dyspepsia Management

Published on: June 29, 2019

An Allele-specific Gene Expression Assay to Test the Functional Basis of Genetic Associations
10:17

An Allele-specific Gene Expression Assay to Test the Functional Basis of Genetic Associations

Published on: November 3, 2010

Area of Science:

  • Gastroenterology
  • Human Genetics
  • Molecular Epidemiology

Background:

  • Familial clustering suggests a genetic component in functional dyspepsia (FD).
  • Previous studies on gene polymorphisms and FD susceptibility have yielded inconsistent results.
  • Genetic epidemiology provides a framework for investigating FD's genetic basis.

Purpose of the Study:

  • To review and summarize the existing evidence on the role of genetic factors in functional dyspepsia susceptibility.
  • To highlight inconsistencies in current genetic association studies for FD.

Main Methods:

  • Review of genetic association studies focusing on FD symptom phenotypes.
  • Analysis of candidate gene polymorphisms, including G-protein beta3 (GNB3) and serotonin transporter promoter (SERT-P).
  • Examination of reported associations in various international populations.

Main Results:

  • Limited genetic association studies exist for FD candidate genes; no genome-wide association studies have been conducted.
  • Inconsistent findings reported for GNB3 C825T polymorphism across Germany, USA, Japan, and Netherlands.
  • Conflicting results for SERT-P gene polymorphism association with FD; SERT SL genotype linked to PDS in this study.
  • Japanese studies reported associations with IL-17F, MIF, COMT, CCK-1, COX-1, TRPV1, and RANTES polymorphisms.

Conclusions:

  • Genetic factors are implicated in the development of dyspeptic symptoms.
  • Further research is required to validate these genetic associations.
  • Understanding genetic influences is crucial for elucidating FD's clinical manifestations.