Go to JCI Insight
  • About
  • Editors
  • Consulting Editors
  • For authors
  • Alerts
  • Advertising/recruitment
  • Subscribe
  • Contact
  • Current Issue
  • Past Issues
  • By specialty
    • COVID-19
    • Cardiology
    • Gastroenterology
    • Immunology
    • Metabolism
    • Nephrology
    • Neuroscience
    • Oncology
    • Pulmonology
    • Vascular biology
    • All ...
  • Videos
    • Conversations with Giants in Medicine
    • Author's Takes
  • Reviews
    • View all reviews ...
    • 100th Anniversary of Insulin's Discovery (Jan 2021)
    • Hypoxia-inducible factors in disease pathophysiology and therapeutics (Oct 2020)
    • Latency in Infectious Disease (Jul 2020)
    • Immunotherapy in Hematological Cancers (Apr 2020)
    • Big Data's Future in Medicine (Feb 2020)
    • Mechanisms Underlying the Metabolic Syndrome (Oct 2019)
    • Reparative Immunology (Jul 2019)
    • View all review series ...
  • Viewpoint
  • Collections
    • Recently published
    • In-Press Preview
    • Commentaries
    • Concise Communication
    • Editorials
    • Viewpoint
    • Top read articles
  • Clinical Medicine
  • JCI This Month
    • Current issue
    • Past issues

  • Current issue
  • Past issues
  • Specialties
  • Reviews
  • Review series
  • Conversations with Giants in Medicine
  • Author's Takes
  • Recently published
  • In-Press Preview
  • Commentaries
  • Concise Communication
  • Editorials
  • Viewpoint
  • Top read articles
  • About
  • Editors
  • Consulting Editors
  • For authors
  • Alerts
  • Advertising/recruitment
  • Subscribe
  • Contact
Glucose-induced β cell production of IL-1β contributes to glucotoxicity in human pancreatic islets
Kathrin Maedler, … , Philippe A. Halban, Marc Y. Donath
Kathrin Maedler, … , Philippe A. Halban, Marc Y. Donath
Published September 15, 2002
Citation Information: J Clin Invest. 2002;110(6):851-860. https://doi.org/10.1172/JCI15318.
View: Text | PDF | Corrigendum
Article Endocrinology

Glucose-induced β cell production of IL-1β contributes to glucotoxicity in human pancreatic islets

  • Text
  • PDF
Abstract

Research Article

Authors

Kathrin Maedler, Pavel Sergeev, Frédéric Ris, José Oberholzer, Helen I. Joller-Jemelka, Giatgen A. Spinas, Nurit Kaiser, Philippe A. Halban, Marc Y. Donath

×

Figure 1

Options: View larger image (or click on image) Download as PowerPoint
Glucose induces IL-1β expression and release in human islets. (a) Secret...
Glucose induces IL-1β expression and release in human islets. (a) Secretion of IL-1β from human islets cultured on extracellular matrix–coated dishes for 4 days in 5.5, 11.1, or 33.3 mM D-glucose or in 5.5 mM D-glucose plus 27.8 mM L-glucose. Each bar represents the mean ± SEM of eight experiments from eight separate donors. *P < 0.01 compared with islets cultured in 5.5 mM glucose alone. (b) Secretion of IL-1β from human islets during 44 hours of culture in suspension with 5.5 or 33.3 mM D-glucose. Data were collected from four tubes per treatment in two separate experiments from two donors. Data are represented as mean ± SEM. *P < 0.01 compared with islets cultured in 5.5 mM glucose. (c) Immunoblotting of pro–IL-1β, IL-1β, and actin. Human islets cultured in suspension at 5.5 or 33.3 mM glucose were analyzed after 44 hours of incubation. One experiment of eleven (from eleven donors) is shown. In seven experiments, glucose induced IL-1β. In three experiments, IL-1β remained unchanged, and in one it was decreased. (d) RT-PCR detection and quantification of IL-1β mRNA expression. Total RNA was isolated from human islets cultured for 44 hours in medium containing 5.5 or 33.3 mM glucose. In the LightCycler quantitative PCR system, the level of IL-1β expression was normalized against GAPDH and the results were expressed as mRNA levels relative to control incubations at 5.5 mM. Results are presented as mean ± SEM for six independent experiments from six donors. *P < 0.05 relative to islets cultured in 5.5 mM glucose.
Follow JCI:
Copyright © 2021 American Society for Clinical Investigation
ISSN: 0021-9738 (print), 1558-8238 (online)

Sign up for email alerts