Evidence map›Paper›PMID 29570955›Full record

ArticleJournal of diabetes investigation2018

Human pancreatic α- to β-cell area ratio increases after type 2 diabetes onset.

Yukari Fujita, Junji Kozawa, Hiromi Iwahashi, Sho Yoneda, Sae Uno, Hidetoshi Eguchi, Hiroaki Nagano, Akihisa Imagawa, Iichiro Shimomura

Open access · goldAbstract read
In one paragraph

Article in Journal of diabetes investigation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
3.3field-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

22 citing papers in PubMed, 30 citations in OpenAlex.

  1. Article
  2. Med14 phosphorylation shapes genomic response to GLP-1 agonists.Proceedings of the National Academy of Sciences of the United States of America · 2026
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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 2 institutions in 1 country.

Yukari FujitaDepartment of Metabolic Medicine, Graduate School of Medicine, Osaka University, Suita, Japan.
Junji KozawaDepartment of Metabolic Medicine, Graduate School of Medicine, Osaka University, Suita, Japan.ORCID http://orcid.org/0000-0001-9665-8947
Hiromi IwahashiDepartment of Metabolic Medicine, Graduate School of Medicine, Osaka University, Suita, Japan.ORCID http://orcid.org/0000-0003-3275-6972
Sho YonedaDepartment of Metabolic Medicine, Graduate School of Medicine, Osaka University, Suita, Japan.
Sae UnoDepartment of Metabolic Medicine, Graduate School of Medicine, Osaka University, Suita, Japan.ORCID http://orcid.org/0000-0003-0565-7311
Hidetoshi EguchiDepartment of Gastroenterological Surgery, Graduate School of Medicine, Osaka University, Suita, Japan.
Hiroaki NaganoDepartment of Gastroenterological Surgery, Graduate School of Medicine, Osaka University, Suita, Japan.
Akihisa ImagawaDepartment of Metabolic Medicine, Graduate School of Medicine, Osaka University, Suita, Japan.
Iichiro ShimomuraDepartment of Metabolic Medicine, Graduate School of Medicine, Osaka University, Suita, Japan.
The University of Osaka · JPOsaka Gakuin University · JP

Funding

Japanese Society for the Promotion of Science 25461350
6 · The paper itself

Abstract

AIMS/

introductionPancreatic α-cell area and the α- to β-cell area ratio (α/β) might be associated with glucose tolerance. The aim was to clarify how these histological parameters change as glucose tolerance deteriorates. MATERIALS AND

methodsWe analyzed pancreatic tissues obtained from pancreatectomies of 43 patients. We evaluated the relationships between α-cell area or the α/β and various clinical parameters. Additionally, we analyzed α-cell proliferation and the expression patterns of various pancreatic transcription factors.

resultsThe α/β in individuals with longstanding (previously diagnosed) type 2 diabetes (0.36 ± 0.12) was higher than that in those with normal glucose tolerance (0.18 ± 0.10; P < 0.01), impaired glucose tolerance (0.17 ± 0.12; P < 0.05) and newly diagnosed diabetes (0.17 ± 0.12; P < 0.05). In all participants, glycated hemoglobin (HbA1c) correlated with relative α-cell area (P = 0.010). Diabetes duration (P = 0.004), HbA1c (P < 0.001) and plasma glucose levels (P = 0.008) were significantly correlated with the α/β in single regression analyses, and diabetes duration was the only independent and significant determinant in stepwise multiple regression analyses (P = 0.006). The α-cell Ki67-positive ratio in patients with HbA1c ≥6.5% was significantly higher than that in patients with HbA1c <6.5% (P = 0.022). We identified β-cells that expressed aristaless-related homeobox and α-cells that did not express aristaless-related homeobox at all glucose tolerance stages. Aristaless-related homeobox and NK homeobox 6.1 expression patterns varied in insulin and glucagon double-positive cells.

conclusionsThe pancreatic α/β increases after type 2 diabetes onset and correlates with diabetes duration. This change might occur through α-cell proliferation and phenotypic changes in pancreatic endocrine cells.

Indexed as

AgedCell ProliferationDiabetes Mellitus, Type 2FemaleGlucagonGlucagon-Secreting CellsGlucose Tolerance TestGlycated HemoglobinHumansInsulin-Secreting CellsMaleMiddle AgedGlucagonGlycated Hemoglobinhemoglobin A1c protein, humanAristaless-related homeoboxα-Cell massα-Cell proliferation

Identifiers

PMID29570955
PMCPMC6215948
OpenAlexW2794060908

What OpenQuestion holds

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LicenceCC BY-NC
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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.