Evidence map›Paper›PMID 27042265›Full record

ReviewJournal of diabetes investigation2016

Dynamic pathology of islet endocrine cells in type 2 diabetes: β-Cell growth, death, regeneration and their clinical implications.

Soroku Yagihashi, Wataru Inaba, Hiroki Mizukami

Abstract readReview
In one paragraph

Review in Journal of diabetes investigation, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
–field-weighted citation impact
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

31 citing papers in PubMed.

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  15. Rs864745 inFrontiers in endocrinology · 2022
    Article
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  17. Review
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  19. Proinsulin is sensitive to reflect glucose intolerance.Journal of diabetes investigation · 2020
    Article
  20. 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

3 authors.

Soroku YagihashiDepartment of Pathology and Molecular Medicine Hirosaki University Graduate School of Medicine Hirosaki Japan.
Wataru InabaDepartment of Pathology and Molecular Medicine Hirosaki University Graduate School of Medicine Hirosaki Japan.
Hiroki MizukamiDepartment of Pathology and Molecular Medicine Hirosaki University Graduate School of Medicine Hirosaki Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Diabetes is defined as a disease of hyperglycemic metabolic disorder caused by impaired insulin action or low insulin secretion, resulting in the occurrence of vascular complications. Based on this definition, diabetes therapy has long been oriented to correct hyperglycemia against the specific complications of diabetes. This definition has posed some difficulties, however, in understanding of the pathophysiology of this complicated disease and as such in the establishment of an effective treatment. With continuing efforts to explore the structural basis for diabetes onset and methodological development of immunohistochemistry, progressive decline of β-cells is now established as a salient feature of type 2 diabetes. Accordingly, diabetes therapy has now turned out to protect β-cells concurrently with the correction of hyperglycemia. Together with this effort, exploration of the means to regenerate β-cells or to supply new β-cells by, for example, induced pluripotential stem cells, are vigorously made with the search for the mechanism of β-cell decline in diabetes. In the present review, we describe the advances in the islet pathology in type 2 diabetes with special reference to the dynamic alterations of islet endocrine cells in the milieu of maturation, obesity, aging and ethnic differences. The effect of amyloid deposition is also discussed. We hope it will help with understanding the pathophysiology of diabetes, and suggest the future direction of diabetes treatment.

Indexed as

AmyloidCell ProliferationCellular SenescenceDiabetes Mellitus, Type 2HumansHyperglycemiaHyperplasiaInsulinInsulin-Secreting CellsIslets of LangerhansModels, BiologicalObesityRegenerationAmyloidInsulinIsletPathologyType 2 diabetes

Identifiers

PMID27042265
PMCPMC4773678

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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.