Evidence map›Paper›PMID 25816051›Full record

Trial reportThe Journal of clinical endocrinology and metabolism2015

Plasma GAD65, a Marker for Early β-Cell Loss After Intraportal Islet Cell Transplantation in Diabetic Patients.

Zhidong Ling, Pieter De Pauw, Daniel Jacobs-Tulleneers-Thevissen, Rui Mao, Pieter Gillard, Christiane S Hampe, Geert A Martens, Peter In't Veld, Åke Lernmark, Bart Keymeulen and 2 more

Open access · bronzeAbstract readClinical Trial
PubMed Full text at PMC Publisher
In one paragraph

Trial report in The Journal of clinical endocrinology and metabolism, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
4.1field-weighted citation impact, top 6% 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

13 citing papers in PubMed, 26 citations in OpenAlex.

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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

12 authors at 4 institutions in 3 countries.

Zhidong LingDiabetes Research Center and Universitair Ziekenhuis Brussel (Z.L., P.D.P., D.J.-T.-T., R.M., G.A.M., P.I.V., B.K., F.G., D.P.), Brussels Free University-VUB, B-1090 Brussels, Belgium; Department of Endocrinology (P.G.), Universitair Ziekenhuis Gasthuisberg, Katholieke Universiteit Leuven-KUL, B-3000 Leuven, Belgium; Department of Medicine (C.S.H.), University of Washington, Seattle, Washington 98109; and Department of Clinical Sciences (Å.L.), Lund University, Skåne University Hospital, SE-20502 Malmö, Sweden.
Pieter De PauwDiabetes Research Center and Universitair Ziekenhuis Brussel (Z.L., P.D.P., D.J.-T.-T., R.M., G.A.M., P.I.V., B.K., F.G., D.P.), Brussels Free University-VUB, B-1090 Brussels, Belgium; Department of Endocrinology (P.G.), Universitair Ziekenhuis Gasthuisberg, Katholieke Universiteit Leuven-KUL, B-3000 Leuven, Belgium; Department of Medicine (C.S.H.), University of Washington, Seattle, Washington 98109; and Department of Clinical Sciences (Å.L.), Lund University, Skåne University Hospital, SE-20502 Malmö, Sweden.
Daniel Jacobs-Tulleneers-ThevissenDiabetes Research Center and Universitair Ziekenhuis Brussel (Z.L., P.D.P., D.J.-T.-T., R.M., G.A.M., P.I.V., B.K., F.G., D.P.), Brussels Free University-VUB, B-1090 Brussels, Belgium; Department of Endocrinology (P.G.), Universitair Ziekenhuis Gasthuisberg, Katholieke Universiteit Leuven-KUL, B-3000 Leuven, Belgium; Department of Medicine (C.S.H.), University of Washington, Seattle, Washington 98109; and Department of Clinical Sciences (Å.L.), Lund University, Skåne University Hospital, SE-20502 Malmö, Sweden.
Rui MaoDiabetes Research Center and Universitair Ziekenhuis Brussel (Z.L., P.D.P., D.J.-T.-T., R.M., G.A.M., P.I.V., B.K., F.G., D.P.), Brussels Free University-VUB, B-1090 Brussels, Belgium; Department of Endocrinology (P.G.), Universitair Ziekenhuis Gasthuisberg, Katholieke Universiteit Leuven-KUL, B-3000 Leuven, Belgium; Department of Medicine (C.S.H.), University of Washington, Seattle, Washington 98109; and Department of Clinical Sciences (Å.L.), Lund University, Skåne University Hospital, SE-20502 Malmö, Sweden.
Pieter GillardDiabetes Research Center and Universitair Ziekenhuis Brussel (Z.L., P.D.P., D.J.-T.-T., R.M., G.A.M., P.I.V., B.K., F.G., D.P.), Brussels Free University-VUB, B-1090 Brussels, Belgium; Department of Endocrinology (P.G.), Universitair Ziekenhuis Gasthuisberg, Katholieke Universiteit Leuven-KUL, B-3000 Leuven, Belgium; Department of Medicine (C.S.H.), University of Washington, Seattle, Washington 98109; and Department of Clinical Sciences (Å.L.), Lund University, Skåne University Hospital, SE-20502 Malmö, Sweden.
Christiane S HampeDiabetes Research Center and Universitair Ziekenhuis Brussel (Z.L., P.D.P., D.J.-T.-T., R.M., G.A.M., P.I.V., B.K., F.G., D.P.), Brussels Free University-VUB, B-1090 Brussels, Belgium; Department of Endocrinology (P.G.), Universitair Ziekenhuis Gasthuisberg, Katholieke Universiteit Leuven-KUL, B-3000 Leuven, Belgium; Department of Medicine (C.S.H.), University of Washington, Seattle, Washington 98109; and Department of Clinical Sciences (Å.L.), Lund University, Skåne University Hospital, SE-20502 Malmö, Sweden.
Geert A MartensDiabetes Research Center and Universitair Ziekenhuis Brussel (Z.L., P.D.P., D.J.-T.-T., R.M., G.A.M., P.I.V., B.K., F.G., D.P.), Brussels Free University-VUB, B-1090 Brussels, Belgium; Department of Endocrinology (P.G.), Universitair Ziekenhuis Gasthuisberg, Katholieke Universiteit Leuven-KUL, B-3000 Leuven, Belgium; Department of Medicine (C.S.H.), University of Washington, Seattle, Washington 98109; and Department of Clinical Sciences (Å.L.), Lund University, Skåne University Hospital, SE-20502 Malmö, Sweden.
Peter In't VeldDiabetes Research Center and Universitair Ziekenhuis Brussel (Z.L., P.D.P., D.J.-T.-T., R.M., G.A.M., P.I.V., B.K., F.G., D.P.), Brussels Free University-VUB, B-1090 Brussels, Belgium; Department of Endocrinology (P.G.), Universitair Ziekenhuis Gasthuisberg, Katholieke Universiteit Leuven-KUL, B-3000 Leuven, Belgium; Department of Medicine (C.S.H.), University of Washington, Seattle, Washington 98109; and Department of Clinical Sciences (Å.L.), Lund University, Skåne University Hospital, SE-20502 Malmö, Sweden.
Åke LernmarkDiabetes Research Center and Universitair Ziekenhuis Brussel (Z.L., P.D.P., D.J.-T.-T., R.M., G.A.M., P.I.V., B.K., F.G., D.P.), Brussels Free University-VUB, B-1090 Brussels, Belgium; Department of Endocrinology (P.G.), Universitair Ziekenhuis Gasthuisberg, Katholieke Universiteit Leuven-KUL, B-3000 Leuven, Belgium; Department of Medicine (C.S.H.), University of Washington, Seattle, Washington 98109; and Department of Clinical Sciences (Å.L.), Lund University, Skåne University Hospital, SE-20502 Malmö, Sweden.
Bart KeymeulenDiabetes Research Center and Universitair Ziekenhuis Brussel (Z.L., P.D.P., D.J.-T.-T., R.M., G.A.M., P.I.V., B.K., F.G., D.P.), Brussels Free University-VUB, B-1090 Brussels, Belgium; Department of Endocrinology (P.G.), Universitair Ziekenhuis Gasthuisberg, Katholieke Universiteit Leuven-KUL, B-3000 Leuven, Belgium; Department of Medicine (C.S.H.), University of Washington, Seattle, Washington 98109; and Department of Clinical Sciences (Å.L.), Lund University, Skåne University Hospital, SE-20502 Malmö, Sweden.
Frans GorusDiabetes Research Center and Universitair Ziekenhuis Brussel (Z.L., P.D.P., D.J.-T.-T., R.M., G.A.M., P.I.V., B.K., F.G., D.P.), Brussels Free University-VUB, B-1090 Brussels, Belgium; Department of Endocrinology (P.G.), Universitair Ziekenhuis Gasthuisberg, Katholieke Universiteit Leuven-KUL, B-3000 Leuven, Belgium; Department of Medicine (C.S.H.), University of Washington, Seattle, Washington 98109; and Department of Clinical Sciences (Å.L.), Lund University, Skåne University Hospital, SE-20502 Malmö, Sweden.
Daniel PipeleersDiabetes Research Center and Universitair Ziekenhuis Brussel (Z.L., P.D.P., D.J.-T.-T., R.M., G.A.M., P.I.V., B.K., F.G., D.P.), Brussels Free University-VUB, B-1090 Brussels, Belgium; Department of Endocrinology (P.G.), Universitair Ziekenhuis Gasthuisberg, Katholieke Universiteit Leuven-KUL, B-3000 Leuven, Belgium; Department of Medicine (C.S.H.), University of Washington, Seattle, Washington 98109; and Department of Clinical Sciences (Å.L.), Lund University, Skåne University Hospital, SE-20502 Malmö, Sweden.
Universitair Ziekenhuis Brussel · BEKU Leuven · BELund University · SEUniversity of Washington · US

Funding

ISLET CELL MEMBRANE ANTIBODIES IN DIABTESR01DK026190 · NIDDK · UNIVERSITY OF WASHINGTON · PI HAMPE, CHRISTIANE S · 1986 to 2016
$4.9M
NIDDK NIH HHS R01 DK026190
6 · The paper itself

Abstract

CONTEXT AND

objectiveIntraportal islet transplantation can restore insulin production in type 1 diabetes patients, but its effect is subject to several interfering processes. To assess the influence of β-cell loss before and during engraftment, we searched for a real-time marker of β-cell destruction. Previous studies showed that 65-kDa isoform of glutamate decarboxylase (GAD65) is discharged by chemically damaged rat β-cells. We therefore examined the utility of the GAD65 assay to detect and quantify destruction of human β-cells in vitro and in vivo. DESIGN AND

participantsA time-resolved fluorescence immunoassay was used to measure GAD65 discharge from β-cells after administration of toxins or after intraportal transplantation. The study in patients involved type 1 diabetes recipients of 56 implants.

resultsGAD65 was discharged from cultured human β-cells between 4 and 24 hours after acute insult and proportional to the number of dying cells. It was also detected in plasma during the first 24 hours after intraportal transplantation of human islet cell grafts. Diabetic nude rat recipients without hyperglycemic correction exhibited higher plasma GAD65 levels than those with normalization. In type 1 diabetes recipients of grafts with 2-5 × 10(6) β-cells per kilogram of body weight, five of six with plasma GAD65 greater than 1 ng/mL failed to increase plasma C-peptide by greater than 0.5 ng/mL at posttransplant month 2, whereas five of six with undetectable plasma GAD 65 and 15 of 19 with intermediate levels did result in such increase.

conclusionPlasma GAD65 qualifies as a marker for early β-cell loss after intraportal transplantation. Further studies are needed to extend its clinical utility.

Indexed as

AnimalsBiomarkersCell DeathCells, CulturedDiabetes Mellitus, ExperimentalDiabetes Mellitus, Type 1Glutamate DecarboxylaseGraft SurvivalHumansInsulin-Secreting CellsIslets of Langerhans TransplantationMalePortal VeinPrognosisRatsRats, NudeBiomarkersGlutamate Decarboxylaseglutamate decarboxylase 2Streptozocin

Identifiers

PMID25816051
PMCPMC5393519
OpenAlexW2184415482

What OpenQuestion holds

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Registered trials

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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.