Evidence map›Paper›PMID 19148619›Full record

ArticleDiabetologia2009

Oxidative stress is induced by islet amyloid formation and time-dependently mediates amyloid-induced beta cell apoptosis.

S Zraika, R L Hull, J Udayasankar, K Aston-Mourney, S L Subramanian, R Kisilevsky, W A Szarek, S E Kahn

Open access · bronzeAbstract read
In one paragraph

Article in Diabetologia, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 116 papers.

0numbers the graph read from it
0cells of the map it votes in
116citing papers in PubMed
13.8field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

116 citing papers in PubMed, 209 citations in OpenAlex.

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  11. Big versus small: The impact of aggregate size in disease.Protein science : a publication of the Protein Society · 2023
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56 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 3 institutions in 2 countries.

S ZraikaDivision of Metabolism, Endocrinology and Nutrition, Department of Medicine, University of Washington and VA Puget Sound Health Care System, 1660 South Columbian Way (151), Seattle, WA 98108, USA. zraikas@u.washington.edu
R L Hull
J Udayasankar
K Aston-Mourney
S L Subramanian
R Kisilevsky
W A Szarek
S E Kahn
University of Washington · USVA Puget Sound Health Care System · USQueen's University · CA

Funding

Vector and Transgenic Mouse CoreP30DK017047 · NIDDK · UNIVERSITY OF WASHINGTON · PI Karin E Bornfeldt · 1986 to 2026
$41.4M
Mechanisms of Islet AmyloidogenesisR01DK075998 · NIDDK · SEATTLE INST FOR BIOMEDICAL/CLINICAL RES · PI KAHN, STEVEN EMANUEL · 2008 to 2011
$1.2M
Role of perlecan in islet amyloid formationK01DK074404 · NIDDK · UNIVERSITY OF WASHINGTON · PI HULL-MEICHLE, REBECCA LUCY · 2006 to 2010
$596k
NIDDK NIH HHS DK-17047NIDDK NIH HHS DK-74404NIDDK NIH HHS DK-75998NIDDK NIH HHS K01 DK074404NIDDK NIH HHS P30 DK017047NIDDK NIH HHS R01 DK075998
6 · The paper itself

Abstract

aims/hypothesisIslet amyloid in type 2 diabetes contributes to loss of beta cell mass and function. Since islets are susceptible to oxidative stress-induced toxicity, we sought to determine whether islet amyloid formation is associated with induction of oxidative stress.

methodsHuman islet amyloid polypeptide transgenic and non-transgenic mouse islets were cultured for 48 or 144 h with or without the antioxidant N-acetyl-L: -cysteine (NAC) or the amyloid inhibitor Congo Red. Amyloid deposition, reactive oxygen species (ROS) production, beta cell apoptosis, and insulin secretion, content and mRNA were measured.

resultsAfter 48 h, amyloid deposition was associated with increased ROS levels and increased beta cell apoptosis, but no change in insulin secretion, content or mRNA levels. Antioxidant treatment prevented the rise in ROS, but did not prevent amyloid formation or beta cell apoptosis. In contrast, inhibition of amyloid formation prevented the induction of oxidative stress and beta cell apoptosis. After 144 h, amyloid deposition was further increased and was associated with increased ROS levels, increased beta cell apoptosis and decreased insulin content. At this time-point, antioxidant treatment and inhibition of amyloid formation were effective in reducing ROS levels, amyloid formation and beta cell apoptosis. Inhibition of amyloid formation also increased insulin content. CONCLUSIONS/

interpretationIslet amyloid formation induces oxidative stress, which in the short term does not mediate beta cell apoptosis, but in the longer term may feed back to further exacerbate amyloid formation and contribute to beta cell apoptosis.

Indexed as

AmyloidAnimalsApoptosisDiabetes Mellitus, Type 2HumansInsulinInsulin-Secreting CellsInsulin SecretionIslet Amyloid PolypeptideMiceMice, TransgenicOxidative StressReactive Oxygen SpeciesRNA, MessengerAmyloidInsulinIslet Amyloid PolypeptideReactive Oxygen SpeciesRNA, Messenger

Identifiers

PMID19148619
PMCPMC2719780
OpenAlexW2056410662

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.