Evidence map›Paper›PMID 25036704›Full record

ArticleThe Journal of clinical investigation2014

Islet amyloid and type 2 diabetes: overproduction or inadequate clearance and detoxification?

Dhananjay Gupta, Jack L Leahy

Open access · bronzeAbstract readComment
In one paragraph

Article in The Journal of clinical investigation, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.3field-weighted citation impact, top 19% 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

11 citing papers in PubMed, 24 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

2 authors.

Dhananjay Gupta
Jack L Leahy

Funding

Beta-Cell Compensation In Partial Pancreatectomy MiceR01DK056818 · NIDDK · UNIVERSITY OF VERMONT &ST AGRIC COLLEGE · PI LEAHY, JOHN L. · 2000 to 2013
$4.0M
Beta-Cell Compensation in Partial Pancreatectomy MiceR56DK056818 · NIDDK · UNIVERSITY OF VERMONT & ST AGRIC COLLEGE · PI LEAHY, JOHN L. · 2008 to 2010
$579k
NIDDK NIH HHS DK56818NIDDK NIH HHS R01 DK056818NIDDK NIH HHS R56 DK056818
6 · The paper itself

Abstract

A hallmark of type 2 diabetes is the reduction of pancreatic islet β cell mass through induction of apoptosis and lack of regeneration. In most patients, β cell dysfunction is associated with the presence of extracellular amyloid plaques adjacent to β cells and intracellular toxic oligomers that are comprised of islet amyloid polypeptide (IAPP). In this issue of the JCI, three independent research groups reveal that a functional autophagy system normally prevents the accumulation of toxic IAPP oligomers in human IAPP-expressing murine models. Furthermore, mice expressing human IAPP but deficient for β cell autophagy through genetic deletion of the autophagy initiator ATG7 developed β cell apoptosis and overt diabetes. Together, these studies indicate that autophagy protects β cells from the accumulation of toxic IAPP oligomers and suggest that enhancing autophagy may be a novel target for prevention of type 2 diabetes.

Indexed as

AnimalsAutophagyDiabetes Mellitus, Type 2FemaleHumansInsulin-Secreting CellsIslet Amyloid PolypeptideMaleIslet Amyloid Polypeptide

Identifiers

PMID25036704
PMCPMC4109527
OpenAlexW2140661828

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.