Evidence map›Paper›PMID 30767048›Full record

ReviewDiabetologia2019

Beta cells in type 1 diabetes: mass and function; sleeping or dead?

Richard A Oram, Emily K Sims, Carmella Evans-Molina

Open access · hybridAbstract readReview
In one paragraph

Review in Diabetologia, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 86 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
86citing papers in PubMed, 1 pooled it
18.3field-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

86 citing papers in PubMed, 1 synthesis or guideline pooled it, 136 citations in OpenAlex.

  1. Pooled it
  2. Residual Corticosteroid Production in Autoimmune Addison Disease.The Journal of clinical endocrinology and metabolism · 2020
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26 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 3 institutions in 2 countries.

Richard A OramRILD Level 3, Institute of Biomedical and Clinical Science, University of Exeter Medical School, Royal Devon and Exeter Hospital, Barrack Road, Exeter, EX2 5DW, UK. R.Oram@exeter.ac.uk.
Emily K SimsDepartment of Pediatrics, Indiana University School of Medicine, Indianapolis, IN, USA.
Carmella Evans-MolinaDepartment of Pediatrics, Indiana University School of Medicine, Indianapolis, IN, USA. cevansmo@iu.edu.
Indiana University – Purdue University Indianapolis · USIndiana University School of MedicineRoyal Devon and Exeter Hospital · GB

Funding

Translation CoreP30DK097512 · NIDDK · INDIANA UNIVERSITY INDIANAPOLIS · PI JEFFREY S ELMENDORF · 2015 to 2026
$17.4M
Mechanisms of Beta Cell Function in Health and DiseaseR01DK093954 · NIDDK · INDIANA UNIVERSITY INDIANAPOLIS · PI EVANS-MOLINA, CARMELLA · 2011 to 2019
$3.5M
Biomarkers Of Beta Cell Stress In Type 1 Diabetes (BetaMarker)UC4DK104166 · NIDDK · INDIANA UNIVERSITY INDIANAPOLIS · PI EIZIRIK, DECIO LAKS, EVANS-MOLINA, CARMELLA · 2014 to 2014
$2.4M
Beta cell Derived miR-21 as an Intrinsic Protective Response and Biomarker in Type 1 DiabetesK08DK103983 · NIDDK · INDIANA UNIVERSITY INDIANAPOLIS · PI SIMS, EMILY K · 2014 to 2018
$761k
Regulation of Calcium Homeostasis in the Pancreatic Beta CellI01BX001733 · VA · RLR VA MEDICAL CENTER · PI Carmella Evans-Molina · 2013 to 2026
–
BLRD VA I01 BX001733Medical Research Council MR/P010695/1NIDDK NIH HHS K08 DK103983NIDDK NIH HHS P30 DK097512NIDDK NIH HHS R01 DK093954NIDDK NIH HHS UC4 DK104166
6 · The paper itself

Abstract

Histological analysis of donor pancreases coupled with measurement of serum C-peptide in clinical cohorts has challenged the idea that all beta cells are eventually destroyed in type 1 diabetes. These findings have raised a number of questions regarding how the remaining beta cells have escaped immune destruction, whether pools of 'sleeping' or dysfunctional beta cells could be rejuvenated and whether there is potential for new growth of beta cells. In this Review, we describe histological and in vivo evidence of persistent beta cells in type 1 diabetes and discuss the limitations of current methods to distinguish underlying beta cell mass in comparison with beta cell function. We highlight that evidence for new beta cell growth in humans many years from diagnosis is limited, and that this growth may be very minimal if at all present. We review recent contributions to the debate around beta cell abnormalities contributing to the pathogenesis of type 1 diabetes. We also discuss evidence for restoration of beta cell function, as opposed to mass, in recent-onset type 1 diabetes, but highlight the absence of data supporting functional recovery in the setting of long-duration diabetes. Finally, future areas of research are suggested to help resolve the source and phenotype of residual beta cells that persist in some, but not all, people with type 1 diabetes.

Indexed as

BiomarkersC-PeptideDiabetes Mellitus, Type 1HumansInsulinInsulin-Secreting CellsPancreasPhenotypeResearch DesignBiomarkersC-PeptideInsulinBeta cell functionBeta cell massC-peptideNetwork for Pancreatic Organ Donors with DiabetesProinsulinReviewType 1 diabetes

Identifiers

PMID30767048
PMCPMC6688846
OpenAlexW2912804279

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.