Evidence map›Paper›PMID 19246534›Full record

ArticleEndocrinology2009

Persistent oxidative stress due to absence of uncoupling protein 2 associated with impaired pancreatic beta-cell function.

Jingbo Pi, Yushi Bai, Kiefer W Daniel, Dianxin Liu, Otis Lyght, Diane Edelstein, Michael Brownlee, Barbara E Corkey, Sheila Collins

Open access · bronzeAbstract read
In one paragraph

Article in Endocrinology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 84 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
84citing papers in PubMed, 1 pooled it
12.3field-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

84 citing papers in PubMed, 1 synthesis or guideline pooled it, 161 citations in OpenAlex.

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24 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 5 institutions in 1 country.

Jingbo PiDivision of Translational Biology, The Hamner Institutes for Health Sciences, Research Triangle Park, North Carolina 27709, USA. jpi@thehamner.org
Yushi Bai
Kiefer W Daniel
Dianxin Liu
Otis Lyght
Diane Edelstein
Michael Brownlee
Barbara E Corkey
Sheila Collins
The Hamner Institutes for Health Sciences · USAlbert Einstein College of Medicine · USBoston University · USDuke Medical Center · USThe Bronx Defenders · US

Funding

METABOLIC SIGNAL TRANSDUCTION IN ADIPOCYTESR01DK056690 · NIDDK · BOSTON MEDICAL CENTER · PI CORKEY, BARBARA E., SHIRIHAI, ORIAN S · 2001 to 2015
$6.3M
METABOLIC REGULATION OF INSULIN SECRETIONR01DK035914 · NIDDK · UNIVERSITY OF PENNSYLVANIA · PI CORKEY, BARBARA E., SHIRIHAI, ORIAN S · 1986 to 2013
$5.3M
Paradoxical roles of Nrf2 activation in arsenic-induced beta-cell dysfunctionR01ES016005 · NIEHS · THE HAMNER INSTITUTES · PI PI, JINGBO · 2008 to 2012
$2.5M
MECHANISMS REGULATING EXPRESSION OF THE UCP2 GENER01DK054024 · NIDDK · THE HAMNER INSTITUTES · PI COLLINS, SHEILA · 1998 to 2005
$1.4M
Metabolic Regulation of Insulin SecretionR56DK035914 · NIDDK · BOSTON MEDICAL CENTER · PI CORKEY, BARBARA E., SHIRIHAI, ORIAN S · 2009 to 2009
$500k
Paradoxical Roles of Reactive Oxygen Species in Pancreatic Beta-Cell FunctionK01DK076788 · NIDDK · THE HAMNER INSTITUTES · PI PI, JINGBO · 2007 to 2009
$358k
METABOLIC REGULATION OF INSULIN SECRETIONR37DK035914 · NIDDK · BOSTON UNIVERSITY MEDICAL CENTER HOSP · PI CORKEY, BARBARA E. · 1991 to 1998
–
NIDDK NIH HHS DK35914NIDDK NIH HHS DK54024NIDDK NIH HHS DK76788NIDDK NIH HHS K01 DK076788NIDDK NIH HHS R01 DK035914NIDDK NIH HHS R01 DK054024NIDDK NIH HHS R01 DK056690NIDDK NIH HHS R56 DK035914NIEHS NIH HHS ES016005NIEHS NIH HHS R01 ES016005
6 · The paper itself

Abstract

Uncoupling protein (UCP) 2 is a widely expressed mitochondrial protein whose precise function is still unclear but has been linked to mitochondria-derived reactive oxygen species production. Thus, the chronic absence of UCP2 has the potential to promote persistent reactive oxygen species accumulation and an oxidative stress response. Here, we show that Ucp2-/- mice on three highly congenic (N >10) strain backgrounds (C57BL/6J, A/J, 129/SvImJ), including two independently generated sources of Ucp2-null animals, all exhibit increased oxidative stress. Ucp2-null animals exhibit a decreased ratio of reduced glutathione to its oxidized form in blood and tissues that normally express UCP2, including pancreatic islets. Islets from Ucp2-/- mice exhibit elevated levels of numerous antioxidant enzymes, increased nitrotyrosine and F4/80 staining, but no change in insulin content. Contrary to results in Ucp2-/- mice of mixed 129/B6 strain background, glucose-stimulated insulin secretion in Ucp2-/- islets of each congenic strain was significantly decreased. These data show that the chronic absence of UCP2 causes oxidative stress, including in islets, and is accompanied by impaired glucose-stimulated insulin secretion.

Indexed as

AnimalsGlucoseGlutathioneGlutathione DisulfideInsulinInsulin-Secreting CellsInsulin SecretionIon ChannelsMiceMitochondrial ProteinsOxidative StressReactive Oxygen SpeciesUncoupling Protein 2GlucoseGlutathioneGlutathione DisulfideInsulinIon ChannelsMitochondrial ProteinsReactive Oxygen SpeciesUcp2 protein, mouseUncoupling Protein 2

Identifiers

PMID19246534
PMCPMC2703519
OpenAlexW2051505012

What OpenQuestion holds

Textmetadata
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.