CoChat
Sign Up
Cited by 444Pancreatic function and diabetesEndoplasmic Reticulum Stress and DiseaseDiabetes Treatment and Management

Mechanisms of β-Cell Death in Type 2 Diabetes

Open access
Donath, Marc Y., Ehses, Jan A., Maedler, Kathrin, Schumann, Desiree M., Ellingsgaard, Helga, Eppler, Elisabeth, Reinecke, Manfred·2005·Diabetes
DOI 10.2337/diabetes.54.suppl_2.s108
Open this paper in CoChat — free accountOpen PDF

Abstract

A decrease in the number of functional insulin-producing β-cells contributes to the pathophysiology of type 2 diabetes. Opinions diverge regarding the relative contribution of a decrease in β-cell mass versus an intrinsic defect in the secretory machinery. Here we review the evidence that glucose, dyslipidemia, cytokines, leptin, autoimmunity, and some sulfonylureas may contribute to the maladaptation of β-cells. With respect to these causal factors, we focus on Fas, the ATP-sensitive K+ channel, insulin receptor substrate 2, oxidative stress, nuclear factor-κB, endoplasmic reticulum stress, and mitochondrial dysfunction as their respective mechanisms of action. Interestingly, most of these factors are involved in inflammatory processes in addition to playing a role in both the regulation of β-cell secretory function and cell turnover. Thus, the mechanisms regulating β-cell proliferation, apoptosis, and function are inseparable processes.

Integrity signals

Registry

Crossref · 10.2337/diabetes.54.suppl_2.s108

Cites

7 of 7 references verified0 citation errors · 0 not checkable

Statistics

Recomputing p-values needs the paper’s full text.

Claims the paper makes

We couldn’t retrieve this paper’s full text, so its claims and self-check weren’t run. The registry and citation checks still apply.

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • The proinflammatory cytokines, such as IL-1β, IFN-γ, and TNF-α, inhibit glucose-stimulated insulin secretion and proliferation of beta-cells.

    “The proinflammatory cytokines, such as interleukin-1 beta (IL-1β), interferon gamma (IFN-γ), and tumor necrosis factor alpha (TNF-α), inhibit glucose-stimulated insulin secretion and proliferation of beta-cells [40–42].”

    From Anti-Inflammatory Effects of GLP-1-Based Therapies beyond Glucose Control (2016) · cites this paper as [42]

Cites

Flagged first, then by citations

Cited by

Sorted by citations

Authors
Donath, M. Y., Ehses, J. A., Maedler, K., Schumann, D. M., Ellingsgaard, H., Eppler, E., & Reinecke, M.
Affiliations
  • University Hospital Zurich (CH)
  • Division of Endocrinology and Diabetes, University Hospital Zurich, Zurich, Switzerland
  • University of Zurich (CH)
ORCID
Venue
Diabetes
Publisher
American Diabetes Association
Published
2005-12-01
Volume
54
Issue
suppl_2
Pages
S108-S113
ISSN
  • 0012-1797 (ISSN-L)
  • 1939-327X
DOI
10.2337/diabetes.54.suppl_2.s108
OpenAlex
W2099529905
Cited by
444
References
7
Citations by year
2026: 6 · 2025: 7 · 2024: 7 · 2023: 15 · 2022: 18 · 2021: 29 · 2020: 22 · 2019: 24 · 2018: 24 · 2017: 21 · 2016: 23 · 2015: 33 · 2014: 31 · 2013: 34 · 2012: 36
FWCI
3.79
Type
journal article
Language
en
Open access
Locations
  • Diabetes (publishedVersion)
  • PubMed (publishedVersion)
  • Zurich Open Repository and Archive (University of Zurich) (submittedVersion)
Funders
  • National Science Foundation
  • National Research Foundation
  • Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung (68874)
  • National Institutes of Health
Topics
  • Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Endoplasmic Reticulum Stress and Disease
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Treatment and Management
Keywords
beta-cell death, type 2 diabetes, beta-cell mass, beta-cell apoptosis, beta-cell proliferation, beta-cell dysfunction, Fas, ATP-sensitive potassium channels, insulin receptor substrate 2, oxidative stress, NF-κB, endoplasmic reticulum stress, mitochondrial dysfunction, dyslipidemia, cytokines, leptin, autoimmunity, sulfonylureas, inflammation, insulin secretion
MeSH terms
Animals, Diabetes Mellitus, Type 2, Disease Models, Animal, Humans, Immunity, Innate, Inflammation, Risk Factors, Cell Death, Leptin, Dyslipidemias, Insulin-Secreting Cells

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review