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 Experiment Videos

Does chasing selected 'Fox' to the nucleus prevent diabetes?

Haiyan Wang1, Claes B Wollheim

  • 1Department of Cell Physiology and Metabolism, University Medical Center, CH-1211 Geneva 4, Switzerland. Haiyan.Wang@medicine.unige.ch

Trends in Molecular Medicine
|June 14, 2005
PubMed
Summary
This summary is machine-generated.

Related Concept Videos

You might also read

Related Articles

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

Sort by
Same author

Palmitate impairs autophagic degradation via oxidative stress/perilysosomal Ca2+ overload/mTORC1 activation pathway in pancreatic β cells.

JCI insight·2025
Same author

Harnessing Distinct Tissue-Resident Immune Niches via S100A9/TLR4 Improves Ketone, Lipid, and Glucose Metabolism.

Endocrinology·2025
Same author

Author Correction: Regulation of autophagy by perilysosomal calcium: a new player in β-cell lipotoxicity.

Experimental & molecular medicine·2024
Same author

Regulation of autophagy by perilysosomal calcium: a new player in β-cell lipotoxicity.

Experimental & molecular medicine·2024
Same author

CDN1163, an activator of sarco/endoplasmic reticulum Ca

British journal of pharmacology·2023
Same author

Ablation of GPR56 Causes β-Cell Dysfunction by ATP Loss through Mistargeting of Mitochondrial VDAC1 to the Plasma Membrane.

Biomolecules·2023

Foxa2, a key transcription factor, is inactivated in diabetes, leading to liver issues. Restoring Foxa2 function reversed these problems, suggesting it as a target for obesity and diabetes treatments.

Area of Science:

  • Molecular biology
  • Endocrinology
  • Metabolic diseases

Background:

  • Foxa2 (Hnf3beta) is a transcription factor crucial for glucose and lipid homeostasis in the liver, pancreas, and adipocytes.
  • Hyperinsulinemia can inactivate Foxa2 through nuclear exclusion, contributing to liver steatosis and insulin resistance in diabetes models.

Purpose of the Study:

  • To investigate the role of Foxa2 inactivation in diabetes-related metabolic dysfunction.
  • To evaluate the therapeutic potential of restoring Foxa2 activity.

Main Methods:

  • Utilized three animal models of diabetes.
  • Employed adenovirus-mediated gene delivery to express a constitutively active form of Foxa2 (mutated T156 phosphorylation site).
  • Assessed effects on liver steatosis, insulin resistance, fatty acid oxidation, and biosynthesis.

Related Experiment Videos

Main Results:

  • Hyperinsulinemia-induced Foxa2 nuclear exclusion was linked to liver steatosis and insulin resistance.
  • Adenovirus-mediated expression of active Foxa2 corrected these abnormalities.
  • Active Foxa2 enhanced fatty acid oxidation and reduced fatty acid biosynthesis.

Conclusions:

  • Foxa2 inactivation plays a significant role in the pathogenesis of diet-induced obesity and type 2 diabetes.
  • Preventing Foxa2 phosphorylation is a potential therapeutic strategy for treating metabolic disorders like obesity and diabetes.