Evidence map›Paper›PMID 18971435›Full record

ReviewDiabetes2008

Beta-cell mass and type 1 diabetes: going, going, gone?

Eitan Akirav, Jake A Kushner, Kevan C Herold

Open access · bronzeAbstract readReview
In one paragraph

Review in Diabetes, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
74citing papers in PubMed, 1 pooled it
10.7field-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

74 citing papers in PubMed, 1 synthesis or guideline pooled it, 143 citations in OpenAlex.

  1. Established and emerging biomarkers for the prediction of type 1 diabetes: a systematic review.Translational research : the journal of laboratory and clinical medicine · 2014
    Pooled it
  2. Trial
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  20. Beta Cell Imaging-From Pre-Clinical Validation to First in Man Testing.International journal of molecular sciences · 2020
    Review

14 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

3 authors at 2 institutions in 1 country.

Eitan AkiravDepartment of Immunobiology, Yale University, New Haven, Connecticut, USA.
Jake A Kushner
Kevan C Herold
Yale University · USUniversity of Pennsylvania · US

Funding

Phase II Trial of HOKT3gamma 1 (ALA-ALA) in Type 1 DiabetesR01DK057846 · NIDDK · YALE UNIVERSITY · PI Kevan C Herold · 2000 to 2026
$11.1M
Islet Growth in NOD Mice Tolerant to Autoimmune DiabetesR01DK068678 · NIDDK · YALE UNIVERSITY · PI HEROLD, KEVAN C · 2004 to 2005
$569k
NIDDK NIH HHS DK068678NIDDK NIH HHS DK57846NIDDK NIH HHS R01 DK057846NIDDK NIH HHS R01 DK068678
6 · The paper itself

Abstract

objectiveBeta-cell regeneration is a fundamental but elusive goal for type 1 diabetes research. Our objective is to review newer human and animal studies of beta-cell destruction and regeneration and consider the implications for treatment of type 1 diabetes. RESEARCH DESIGN AND

methodsRecent human and animal studies of beta-cell destruction and regeneration in type 1 diabetes are reviewed.

resultsThe loss of beta-cells that characterizes type 1 diabetes reflects the net effects of destruction and regeneration. These processes have been examined in the nonobese diabetic (NOD) mouse; uncertainty remains about beta-cell dynamics in humans. Islet inflammation stimulates beta-cell replication that produces new insulin-positive cells. The regenerative process may tide the loss of overall beta-cell function, but it also may enhance the autoimmune attack on beta-cells by providing new epitopes. The highest rates of beta-cell replication are at the time of diagnosis of diabetes in NOD mice, and if autoimmunity and islet inflammation are arrested, new beta-cells are formed. However, the majority of beta-cells after treatment with immune modulators such as anti-CD3 monoclonal antibody, and most likely during the "honeymoon" in human disease, are recovered beta-cells that had been degranulated but present at the time of diagnosis of diabetes.

conclusionsResidual beta-cells play a significant role for the design of therapeutic trials: they not only may respond to combination therapies that include stimulants of metabolic function but are also the potential source of new beta-cells.

Indexed as

AnimalsAutoimmunityDiabetes Mellitus, Type 1HumansImmunotherapyInsulin-Secreting CellsMiceModels, Biological

Identifiers

PMID18971435
PMCPMC2570380
OpenAlexW2167255449

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.