Evidence map›Paper›PMID 22396204›Full record

ArticleDiabetes2012

Glycotoxin and autoantibodies are additive environmentally determined predictors of type 1 diabetes: a twin and population study.

Huriya Beyan, Harriette Riese, Mohammed I Hawa, Guisi Beretta, Howard W Davidson, John C Hutton, Huibert Burger, Michael Schlosser, Harold Snieder, Bernhard O Boehm and 1 more

Open access · bronzeAbstract readTwin Study
In one paragraph

Article in Diabetes, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

25 citing papers in PubMed, 60 citations in OpenAlex.

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  10. Similarities and Differences Between HFmrEF and HFpEF.Frontiers in cardiovascular medicine · 2021
    Review
  11. Review
  12. Targeting Glycoproteins as a therapeutic strategy for diabetes mellitus and its complications.Daru : journal of Faculty of Pharmacy, Tehran University of Medical Sciences · 2020
    Review
  13. Review
  14. Article
  15. On type 1 diabetes mellitus pathogenesis.Endocrine connections · 2018
    Review
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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

11 authors at 3 institutions in 3 countries.

Huriya BeyanCentre for Diabetes and Metabolic Medicine, Blizard Institute, Queen Mary, University of London, London, UK.
Harriette Riese
Mohammed I Hawa
Guisi Beretta
Howard W Davidson
John C Hutton
Huibert Burger
Michael Schlosser
Harold Snieder
Bernhard O Boehm
R David Leslie
University Medical Center Groningen · NLUniversity of Colorado Denver · USUniversität Greifswald · DE

Funding

UCHSC DIABETES ENDOCRINOLOGY RESEARCH CENTERP30DK057516 · NIDDK · UNIVERSITY OF COLORADO DENVER · PI HUTTON, JOHN C · 2000 to 2010
$14.0M
MOLECULAR TARGETS OF CMI IN TYPE I DIABETESR01DK052068 · NIDDK · UNIVERSITY OF COLORADO DENVER · PI DAVIDSON, HOWARD W · 1997 to 2014
$3.1M
NIDDK NIH HHS P30 DK057516NIDDK NIH HHS P30-DK-57516NIDDK NIH HHS R01 DK052068NIDDK NIH HHS R01-DK-052068
6 · The paper itself

Abstract

In type 1 diabetes, diabetes-associated autoantibodies, including islet cell antibodies (ICAs), reflect adaptive immunity, while increased serum N(ε)-carboxymethyl-lysine (CML), an advanced glycation end product, is associated with proinflammation. We assessed whether serum CML and autoantibodies predicted type 1 diabetes and to what extent they were determined by genetic or environmental factors. Of 7,287 unselected schoolchildren screened, 115 were ICA(+) and were tested for baseline CML and diabetes autoantibodies and followed (for median 7 years), whereas a random selection (n = 2,102) had CML tested. CML and diabetes autoantibodies were determined in a classic twin study of twin pairs discordant for type 1 diabetes (32 monozygotic, 32 dizygotic pairs). CML was determined by enzyme-linked immunosorbent assay, autoantibodies were determined by radioimmunoprecipitation, ICA was determined by indirect immunofluorescence, and HLA class II genotyping was determined by sequence-specific oligonucleotides. CML was increased in ICA(+) and prediabetic schoolchildren and in diabetic and nondiabetic twins (all P < 0.001). Elevated levels of CML in ICA(+) children were a persistent, independent predictor of diabetes progression, in addition to autoantibodies and HLA risk. In twins model fitting, familial environment explained 75% of CML variance, and nonshared environment explained all autoantibody variance. Serum CML, a glycotoxin, emerged as an environmentally determined diabetes risk factor, in addition to autoimmunity and HLA genetic risk, and a potential therapeutic target.

Indexed as

AdolescentAdultAntibody SpecificityAutoantibodiesChildDiabetes Mellitus, Type 1Enzyme-Linked Immunosorbent AssayFemaleGlycation End Products, AdvancedHumansLysineMalePopulation SurveillanceRadioimmunoprecipitation AssayTwins, DizygoticTwins, MonozygoticAutoantibodiesGlycation End Products, Advancedislet cell antibodyLysineN(6)-carboxymethyllysine

Identifiers

PMID22396204
PMCPMC3331747
OpenAlexW2409449647

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.