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
  1. Home
  3. Research Domains

Activation of nuclear hormone receptor peroxisome proliferator-activated receptor-delta accelerates intestinal adenoma growth.

Rajnish A Gupta1, Dingzhi Wang, Sharada Katkuri

  • 1Department of Medicine, The Vanderbilt-Ingram Cancer Center, Vanderbilt University School of Medicine, Nashville, Tennessee 37232-6838, USA.

Nature Medicine
|February 6, 2004

Related Experiment Videos

View abstract on PubMed

Summary

Related Concept Videos

  • Biomedical And Clinical Sciences
  • Oncology And Carcinogenesis
  • Predictive And Prognostic Markers
  • Activation Of Nuclear Hormone Receptor Peroxisome Proliferator-activated Receptor-delta Accelerates Intestinal Adenoma Growth.
    • This summary is machine-generated.

    Activating peroxisome proliferator-activated receptor-delta (PPAR-delta) significantly increased intestinal polyp growth in mice. This suggests PPAR-delta plays a key role in regulating the development of intestinal adenomas.

    Area of Science:

    • Gastroenterology
    • Molecular Biology
    • Oncology

    Background:

    • Apc(min) mice are a model for studying intestinal polyposis.
    • Peroxisome proliferator-activated receptor-delta (PPAR-delta) is a nuclear receptor with known roles in metabolism and inflammation.

    Purpose of the Study:

    • To investigate the role of PPAR-delta in intestinal adenoma development.
    • To determine the effect of a selective PPAR-delta agonist on polyp growth in Apc(min) mice.

    Main Methods:

    • Treatment of Apc(min) mice with GW501516, a selective synthetic agonist of PPAR-delta.
    • Quantification of intestinal polyp number and size.

    Main Results:

    • PPAR-delta activation led to a significant increase in both the number and size of intestinal polyps.
    • A fivefold increase in polyps larger than 2 mm was observed in treated mice.
    • The most pronounced effect was on polyp size, indicating a role in adenoma growth.

    Conclusions:

    • PPAR-delta signaling is implicated in the regulation of intestinal adenoma growth.
    • Targeting PPAR-delta may represent a potential therapeutic strategy for intestinal polyposis.

    Related Experiment Videos