Evidence map›Paper›PMID 34983671›Full record

ArticleClinical diabetes and endocrinology2022

Heterogeneity of beta-cell function in subjects with multiple islet autoantibodies in the TEDDY family prevention study - TEFA.

Maria Månsson Martinez, Lampros Spiliopoulos, Falastin Salami, Daniel Agardh, Jorma Toppari, Åke Lernmark, Jukka Kero, Riitta Veijola, Päivi Tossavainen, Sauli Palmu and 8 more

Registry-linked trialOpen access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Clinical diabetes and endocrinology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT02605148 (TEFA TEDDY Family Prevention - Gluten Free Diet to Preserve Beta-cell Function in Subjects With Islet Autoimmunity.), which is not on this map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.3field-weighted citation impact, top 31% 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.

NCT02605148 naunknown statusnot on this map

TEFA TEDDY Family Prevention - Gluten Free Diet to Preserve Beta-cell Function in Subjects With Islet Autoimmunity.

TypeinterventionalSponsorLund UniversityRan2015 to 2022Enrolled60ConditionsPrediabetes, Type 1 DiabetesArmsGluten free diet, Omega 3 fatty acid, Vitamin D, Probiotics
3 · Its place in the literature

Who cites it

1 citing paper in PubMed, 3 citations in OpenAlex.

  1. Article
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

18 authors at 5 institutions in 2 countries.

Maria Månsson Martinez *Department of Clinical Sciences, Lund University CRC, Skåne University Hospital, Jan Waldenströms gata 35, Box 503 32, SE-214 28, Malmö, Sweden. maria.mansson_martinez@med.lu.se.ORCID http://orcid.org/0000-0002-3320-1226
Lampros Spiliopoulos *Department of Clinical Sciences, Lund University CRC, Skåne University Hospital, Jan Waldenströms gata 35, Box 503 32, SE-214 28, Malmö, Sweden.
Falastin SalamiDepartment of Clinical Sciences, Lund University CRC, Skåne University Hospital, Jan Waldenströms gata 35, Box 503 32, SE-214 28, Malmö, Sweden.
Daniel AgardhDepartment of Clinical Sciences, Lund University CRC, Skåne University Hospital, Jan Waldenströms gata 35, Box 503 32, SE-214 28, Malmö, Sweden.
Jorma ToppariDepartment of Pediatrics, Turku University Hospital, Turku, Finland.
Åke LernmarkDepartment of Clinical Sciences, Lund University CRC, Skåne University Hospital, Jan Waldenströms gata 35, Box 503 32, SE-214 28, Malmö, Sweden.
Jukka KeroDepartment of Pediatrics, Turku University Hospital, Turku, Finland.
Riitta VeijolaDepartment of Pediatrics, PEDEGO Research Unit, MRC Oulu, University of Oulu, Oulu, Finland.
Päivi TossavainenDepartment of Pediatrics, PEDEGO Research Unit, MRC Oulu, University of Oulu, Oulu, Finland.
Sauli PalmuDepartment of Pediatrics, Tampere Center for Child, Adolescent and Maternal Health Research, Tampere University Hospital, Tampere, Finland.
Markus LundgrenDepartment of Clinical Sciences, Lund University CRC, Skåne University Hospital, Jan Waldenströms gata 35, Box 503 32, SE-214 28, Malmö, Sweden.
Henrik BorgDepartment of Clinical Sciences, Lund University CRC, Skåne University Hospital, Jan Waldenströms gata 35, Box 503 32, SE-214 28, Malmö, Sweden.
Anastasia KatsarouDepartment of Clinical Sciences, Lund University CRC, Skåne University Hospital, Jan Waldenströms gata 35, Box 503 32, SE-214 28, Malmö, Sweden.
Helena Elding LarssonDepartment of Clinical Sciences, Lund University CRC, Skåne University Hospital, Jan Waldenströms gata 35, Box 503 32, SE-214 28, Malmö, Sweden.
Mikael KnipResearch Program for Clinical and Molecular Metabolism, Faculty of Medicine, University of Helsinki, Helsinki, Finland.
Marlena Maziarz *Department of Clinical Sciences, Lund University CRC, Skåne University Hospital, Jan Waldenströms gata 35, Box 503 32, SE-214 28, Malmö, Sweden.
Carina Törn *Department of Clinical Sciences, Lund University CRC, Skåne University Hospital, Jan Waldenströms gata 35, Box 503 32, SE-214 28, Malmö, Sweden.
and the TEDDY-Family (TEFA) Study Group
Lund University · SEOulu University Hospital · FIUniversity of Turku · FITampere University Hospital · FIUniversity of Helsinki · FI

Funding

The Environmental Triggers of Diabetes (TEDDY) in SwedenU01DK063861 · NIDDK · UNIVERSITY OF WASHINGTON · PI LERNMARK, AKE · 2003 to 2022
$13.4M
NIDDK NIH HHS U01 DK063861
6 · The paper itself

Abstract

backgroundIndividuals with multiple islet autoantibodies are at increased risk for clinical type 1 diabetes and may proceed gradually from stage to stage complicating the recruitment to secondary prevention studies. We evaluated multiple islet autoantibody positive subjects before randomisation for a clinical trial 1 month apart for beta-cell function, glucose metabolism and continuous glucose monitoring (CGM). We hypothesized that the number and type of islet autoantibodies in combination with different measures of glucose metabolism including fasting glucose, HbA1c, oral glucose tolerance test (OGTT), intra venous glucose tolerance test (IvGTT) and CGM allows for more precise staging of autoimmune type 1 diabetes than the number of islet autoantibodies alone.

methodsSubjects (n = 57) at 2-50 years of age, positive for two or more islet autoantibodies were assessed by fasting plasma insulin, glucose, HbA1c as well as First Phase Insulin Response (FPIR) in IvGTT, followed 1 month later by OGTT, and 1 week of CGM (n = 24).

resultsAutoantibodies against GAD65 (GADA; n = 52), ZnT8 (ZnT8A; n = 40), IA-2 (IA-2A; n = 38) and insulin (IAA; n = 28) were present in 9 different combinations of 2-4 autoantibodies. Fasting glucose and HbA1c did not differ between the two visits. The estimate of the linear relationship between log2-transformed FPIR as the outcome and log2-transformed area under the OGTT glucose curve (AUC) as the predictor, adjusting for age and sex was - 1.88 (- 2.71, - 1.05) p = 3.49 × 10-5. The direction of the estimates for all glucose metabolism measures was positive except for FPIR, which was negative. FPIR was associated with higher blood glucose. Both the median and the spread of the CGM glucose data were significantly associated with higher glucose values based on OGTT, higher HbA1c, and lower FPIR. There was no association between glucose metabolism, autoantibody number and type except that there was an indication that the presence of at least one of ZnT8(Q/R/W) A was associated with a lower log2-transformed FPIR (- 0.80 (- 1.58, - 0.02), p = 0.046).

conclusionsThe sole use of two or more islet autoantibodies as inclusion criterion for Stage 1 diabetes in prevention trials is unsatisfactory. Staging type 1 diabetes needs to take the heterogeneity in beta-cell function and glucose metabolism into account.

trial registrationClinicalTrials.gov identifier: NCT02605148 , November 16, 2015.

Indexed as

beta-cell functionContinuous glucose monitoringGlucose metabolismIslet autoantibodies

Identifiers

PMID34983671
PMCPMC8728995
OpenAlexW4225332986

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Registered trials

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.