Evidence map›Paper›PMID 22080915›Full record

ArticleCell transplantation2012

Metabolic function of a suboptimal transplanted islet mass in nonhuman primates on rapamycin monotherapy.

Scott A Soleimanpour, Boaz Hirshberg, David J Bunnell, Anne E Sumner, Marilyn Ader, Alan T Remaley, Kristina I Rother, Michael R Rickels, David M Harlan

Open access · bronzeAbstract read
In one paragraph

Article in Cell transplantation, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.6field-weighted citation impact, top 28% 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

5 citing papers in PubMed, 6 citations in OpenAlex.

  1. Improvement in insulin sensitivity after human islet transplantation for type 1 diabetes.The Journal of clinical endocrinology and metabolism · 2013
    Trial
  2. Review
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  4. 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

9 authors at 4 institutions in 1 country.

Scott A SoleimanpourIslet and Autoimmunity Branch, NIDDK, NIH, Bethesda, MD, USA. scott.soleimanpour@uphs.upenn.edu
Boaz Hirshberg
David J Bunnell
Anne E Sumner
Marilyn Ader
Alan T Remaley
Kristina I Rother
Michael R Rickels
David M Harlan
National Institutes of Health · USNational Institute of Diabetes and Digestive and Kidney Diseases · USUniversity of Pennsylvania · USUniversity of Southern California · US

Funding

Secondary Prevention Trials For Recently Diagnosed Type 1 Diabetes MellitusZIADK062001 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI REITMAN, MARC L · 2009 to 2012
$698k
Intramural NIH HHS Z99 DA999999Intramural NIH HHS Z99 DK999999Intramural NIH HHS Z99 OD999999
6 · The paper itself

Abstract

Although islet transplantation may restore insulin independence to individuals with type 1 diabetes mellitus, most have abnormal glucose tolerance. We asked whether the defective glucose tolerance is due to inadequate β-cell mass or to impaired insulin sensitivity. We performed metabolic studies on four cynomolgus primates before inducing diabetes with streptozotocin (STZ), then again 2-3 weeks after restoring insulin independence via intrahepatic islet transplantation utilizing a calcineurin inhibitor-free immunosuppressive regimen (induction with rabbit antithymocyte globulin and maintenance therapy with rapamycin). Engrafted β-cell mass was assessed by acute insulin and C-peptide responses to glucose (AIR(glu) and ACR(glu)) and arginine (AIR(arg) and ACR(arg)). Insulin sensitivity (S(I)) was determined in naive and transplanted primates from an intravenous glucose tolerance test using the minimal model. α-Cell function was determined by the acute glucagon response to arginine (AGR(arg)). Glucose tolerance (K(g)) decreased from 4.1 ± 0.5%/min in naive primates to 1.8 ± 0.3%/min in transplanted primates (p < 0.01). Following transplantation, AIR(glu) was 28.7 ± 13.1 μU/ml compared to 169.9 ± 43.1 μU/ml (p < 0.03) in the naive condition, ACR(glu) was 14.5 ± 6.0 ng/ml compared to 96.5 ± 17.0 ng/ml naive (p < 0.01), AIR(arg) was 29.1 ± 13.1 μU/ml compared to 91.4 ± 28.2 μU/ml naive (p < 0.05), and ACR(arg) was 1.11 ± 0.51 ng/ml compared to 2.79 ± 0.77 ng/ml naive (p < 0.05). S(I) did not differ from naive to posttransplant states. AGR(arg) was reduced in transplanted primates (349 ± 118 pg/ml) when compared to both naive (827 ± 354 pg/ml) and post-STZ diabetic primates (1020 ± 440 pg/ml) (p < 0.01 for both comparisons). These data suggest that impaired glucose tolerance observed in islet transplant recipients is secondary to low functional β-cell mass and not to insulin resistance shortly after transplant. Furthermore, improved glycemic control achieved via islet transplantation over the diabetic state might be attained, in part, via reduced glucagon secretion.

Indexed as

Islets of Langerhans TransplantationAnimalsArginineBlood GlucoseC-PeptideDiabetes Mellitus, ExperimentalGlucagonGlucose Tolerance TestImmunosuppressive AgentsInsulinInsulin-Secreting CellsMacaca fascicularisSirolimusArginineBlood GlucoseC-PeptideGlucagonImmunosuppressive AgentsInsulinSirolimus

Identifiers

PMID22080915
PMCPMC3508173
OpenAlexW2031314935

What OpenQuestion holds

Textmetadata
LicenceTDM
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.