Evidence map›Paper›PMID 20566664›Full record

ArticleDiabetes2010

Targeted disruption of pancreatic-derived factor (PANDER, FAM3B) impairs pancreatic beta-cell function.

Claudia E Robert-Cooperman, Jason R Carnegie, Camella G Wilson, Jichun Yang, Joshua R Cook, Jianmei Wu, Robert A Young, Bryan A Wolf, Brant R Burkhardt

Erratum issuedOpen access · bronzeAbstract read
In one paragraph

Article in Diabetes, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 20 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 1 pooled it
5.0field-weighted citation impact, top 5% 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

20 citing papers in PubMed, 1 synthesis or guideline pooled it, 43 citations in OpenAlex.

  1. Pooled it
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  20. Cytokines in the Progression of Pancreatic β-Cell Dysfunction.International journal of endocrinology · 2010
    Article
4 · The record

Corrections and comments

  • Erratum issued
5 · Who and what money

Authors and funding

9 authors at 2 institutions in 1 country.

Claudia E Robert-CoopermanDepartment of Pathology and Laboratory Medicine, The Children’s Hospital of Philadelphia Research Institute, Philadelphia, Pennsylvania, USA.
Jason R Carnegie
Camella G Wilson
Jichun Yang
Joshua R Cook
Jianmei Wu
Robert A Young
Bryan A Wolf
Brant R Burkhardt
Children's Hospital of Philadelphia · USUniversity of Pennsylvania · US

Funding

VIRAL VECTOR COREP30DK019525 · NIDDK · UNIVERSITY OF PENNSYLVANIA · PI DOUGLAS J EPSTEIN · 1986 to 2026
$48.3M
Mechanism of PANDER Induced ApoptosisK01DK070744 · NIDDK · CHILDREN'S HOSP OF PHILADELPHIA · PI BURKHARDT, BRANT ROGER · 2006 to 2010
$670k
NIDDK NIH HHS DK19525NIDDK NIH HHS K01 DK070744NIDDK NIH HHS K01-DK070744NIDDK NIH HHS P30 DK019525
6 · The paper itself

Abstract

objectivePancreatic-derived factor (PANDER, FAM3B) is a pancreatic islet-specific cytokine-like protein that is secreted from beta-cells upon glucose stimulation. The biological function of PANDER is unknown, and to address this we generated and characterized a PANDER knockout mouse. RESEARCH DESIGN AND

methodsTo generate the PANDER knockout mouse, the PANDER gene was disrupted and its expression was inhibited by homologous recombination via replacement of the first two exons, secretion signal peptide and transcriptional start site, with the neomycin gene. PANDER(-/-) mice were then phenotyped by a number of in vitro and in vivo tests to evaluate potential effects on glucose regulation, insulin sensitivity, and beta-cell morphology and function.

resultsGlucose tolerance tests demonstrated significantly higher blood glucose levels in PANDER(-/-) versus wild-type male mice. To identify the mechanism of the glucose intolerance, insulin sensitivity and pancreatic beta-cell function were examined. Hyperinsulinemic-euglycemic clamps and insulin tolerance testing showed similar insulin sensitivity for both the PANDER(-/-) and wild-type mice. The in vivo insulin response following intraperitoneal glucose injection surprisingly produced significantly higher insulin levels in the PANDER(-/-) mice, whereas insulin release was blunted with arginine administration. Islet perifusion and calcium imaging studies showed abnormal responses of the PANDER(-/-) islets to glucose stimulation. In contrast, neither islet architecture nor insulin content was impacted by the loss of PANDER. Interestingly, the elevated insulin levels identified in vivo were attributed to decreased hepatic insulin clearance in the PANDER(-/-) islets. Taken together, these results demonstrated decreased pancreatic beta-cell function in the PANDER(-/-) mouse.

conclusionsThese results support a potential role of PANDER in the pancreatic beta-cell for regulation or facilitation of insulin secretion.

Indexed as

Adenosine DiphosphateAdenosine TriphosphateAnimalsArginineBlood GlucoseCytokinesDNA PrimersGene AmplificationGlucagon-Like Peptide 1GlucoseGlucose Clamp TechniqueGlucose Tolerance TestInsulinInsulin-Secreting CellsInsulin SecretionMaleAdenosine DiphosphateAdenosine TriphosphateArginineBlood GlucoseCytokinesDNA PrimersGlucagon-Like Peptide 1GlucoseInsulinPANDER protein, mouse

Identifiers

PMID20566664
PMCPMC2927943
OpenAlexW2161114882

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.