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

A radical explanation for glucose-induced beta cell dysfunction.

Michael Brownlee1

  • 1Diabetes Research Center, Albert Einstein College of Medicine, 1300 Morris Park Avenue, New York, New York 10461, USA. Brownlee@aecom.yu.edu

The Journal of Clinical Investigation
|December 18, 2003
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

Rationale of Basic and Cellular Mechanisms Considered in Updating the Staging System for Diabetic Retinal Disease.

Ophthalmology science·2024
Same author

Discovery of PSMA in the prostate of the common marmoset (Callithrix jacchus).

The Prostate·2024
Same author

Malglycemia in the critical care setting. Part III: Temporal patterns, relative potencies, and hospital mortality.

Journal of critical care·2024
Same author

Malglycemia in the critical care setting. Part II: Relative and absolute hypoglycemia.

Journal of critical care·2023
Same author

Malglycemia in the critical care setting. Part I: Defining hyperglycemia in the critical care setting using the glycemic ratio.

Journal of critical care·2023
Same author

Brain Glucose Sensing and the Problem of Relative Hypoglycemia.

Diabetes care·2023
Same journal

Extracellular matrix reprogramming by the YAP/TAZ- TGF-ß2 axis drives immune exclusion in cholangiocarcinoma models.

The Journal of clinical investigation·2026
Same journal

Tumor cell-derived extracellular vesicles foster the immunosuppressive landscape of pancreatic cancer.

The Journal of clinical investigation·2026
Same journal

Julie Zikherman receives the ASCI/Marian W. Ropes, MD, Award.

The Journal of clinical investigation·2026
Same journal

Targeted degradation of MDM2 overcomes feedback regulation of p53 signaling in Merkel cell carcinoma models.

The Journal of clinical investigation·2026
Same journal

SGLT2 inhibitors enhance ketogenesis by acting as allosteric activators of the mitochondrial enzyme HMGCS2.

The Journal of clinical investigation·2026
Same journal

MDM2 degraders for Merkel cell carcinoma: round peg in a round hole.

The Journal of clinical investigation·2026
See all related articles

High blood sugar impairs insulin secretion by activating mitochondrial superoxide production in beta cells. Inhibiting this process may prevent type 2 diabetes progression.

Area of Science:

  • Endocrinology
  • Metabolic diseases
  • Cellular biology

Background:

  • Type 2 diabetes is characterized by impaired beta cell function.
  • Hyperglycemia exacerbates beta cell dysfunction by reducing insulin secretion.

Purpose of the Study:

  • To investigate the mechanism by which hyperglycemia impairs beta cell function.
  • To explore the role of mitochondrial superoxide production and uncoupling protein 2.

Main Methods:

  • The study examined the effects of hyperglycemia on mitochondrial superoxide production in beta cells.
  • Researchers assessed the activation of uncoupling protein 2 and its impact on the ATP/ADP ratio.
  • Insulin secretion response under hyperglycemic conditions was measured.

Related Experiment Videos

Main Results:

  • Hyperglycemia induces mitochondrial superoxide production in beta cells.
  • This superoxide production activates uncoupling protein 2.
  • Uncoupling protein 2 activation lowers the ATP/ADP ratio, reducing insulin secretion.

Conclusions:

  • Hyperglycemia-induced mitochondrial superoxide production creates a feed-forward loop of glucotoxicity.
  • Inhibiting mitochondrial superoxide overproduction could be a therapeutic strategy for type 2 diabetes.
  • Preventing this loop may halt the progression from impaired glucose tolerance to type 2 diabetes.