Evidence map›Paper›PMID 35059256›Full record

ArticleDiabetology international2022

Association of a SNP in the

Ryoichi Kawamura, Yasuharu Tabara, Yasunori Takata, Koutatsu Maruyama, Misaki Takakado, Toshimi Hadate, Yumi Matsushita, Madoka Sano, Hideichi Makino, Isao Saito and 2 more

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Diabetology international, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.2field-weighted citation impact, top 45% 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

1 citing paper in PubMed, 2 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

12 authors at 5 institutions in 1 country.

Ryoichi KawamuraDepartment of Diabetes and Molecular Genetics, Ehime University Graduate School of Medicine, Shitsukawa, Toon, Ehime 791-0295 Japan.
Yasuharu TabaraCenter for Genomic Medicine, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Yasunori TakataDepartment of Diabetes and Molecular Genetics, Ehime University Graduate School of Medicine, Shitsukawa, Toon, Ehime 791-0295 Japan.
Koutatsu MaruyamaDepartment of Bioscience, Graduate School of Agriculture, Ehime University, Matsuyama, Ehime Japan.
Misaki TakakadoDepartment of Diabetes and Molecular Genetics, Ehime University Graduate School of Medicine, Shitsukawa, Toon, Ehime 791-0295 Japan.
Toshimi HadateDepartment of Diabetes and Molecular Genetics, Ehime University Graduate School of Medicine, Shitsukawa, Toon, Ehime 791-0295 Japan.
Yumi MatsushitaDepartment of Diabetes and Molecular Genetics, Ehime University Graduate School of Medicine, Shitsukawa, Toon, Ehime 791-0295 Japan.
Madoka SanoDepartment of Diabetes and Molecular Genetics, Ehime University Graduate School of Medicine, Shitsukawa, Toon, Ehime 791-0295 Japan.
Hideichi MakinoDepartment of Diabetes and Molecular Genetics, Ehime University Graduate School of Medicine, Shitsukawa, Toon, Ehime 791-0295 Japan.
Isao SaitoDepartment of Public Health and Epidemiology, Faculty of Medicine, Oita University, Oita, Japan.
Azuma KanatsukaDiabetes Center, Chiba Central Medical Center, 1835-1 Kasori, Wakaba-ku, Chiba, 264-0017 Japan.
Haruhiko OsawaDepartment of Diabetes and Molecular Genetics, Ehime University Graduate School of Medicine, Shitsukawa, Toon, Ehime 791-0295 Japan.ORCID 0000-0003-0289-8363
Ehime University · JPEhime Medical Center · JPKyoto University · JPOita University · JPTeikyo University Chiba Medical Center · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveIn type 2 diabetes, the significant pathological change in pancreatic islets is amyloid deposits. Its major component is islet amyloid polypeptide (IAPP). The objective of this study was to evaluate the possibility that the effect of the

methodsParticipants from the Toon Genome Study underwent a 75 g OGTT for the diagnosis of glucose tolerance and the evaluation of insulin secretion. We examined the effect of a SNP, rs77397980, on β-cell function by analyzing an interaction (statistics) between the

resultsThe ratio of the C-allele carriers was essentially the same among subjects with normal glucose tolerance, impaired glucose tolerance and diabetes. In subjects with diabetes, along with an increase in AUC glucose, fasting insulin remained constant in the T/T homozygotes and appeared to decrease in the C-allele carriers. A homeostasis model assessment (HOMA)-IR appeared to be increased in the former and decreased in the latter. In subjects with diabetes stratified into cases with higher AUC glucose than the median, fasting insulin and HOMA-IR were lower in the C-allele carriers than in the T/T homozygotes. An interaction between the

conclusionsThe possibility that the association between SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1007/s13340-021-00523-4.

Indexed as

General populationIAPPSNPβ-cell dysfunction

Identifiers

PMID35059256
PMCPMC8733094
OpenAlexW3195430183

What OpenQuestion holds

Textmetadata
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.