Evidence map›Paper›PMID 24843735›Full record

ArticleJournal of diabetes investigation2014

Age-associated changes of islet endocrine cells and the effects of body mass index in Japanese.

Hiroki Mizukami, Kazunori Takahashi, Wataru Inaba, Sho Osonoi, Kosuke Kamata, Kentaro Tsuboi, Soroku Yagihashi

Open access · hybridAbstract read
In one paragraph

Article in Journal of diabetes investigation, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
3.8field-weighted citation impact, top 7% 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

32 citing papers in PubMed, 51 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Article
  6. Review
  7. Review
  8. Article
  9. Article
  10. Biomarkers of aging.Science China. Life sciences · 2023
    Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. Review
  16. Review
  17. Review
  18. Review
  19. Article
  20. Review
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

7 authors at 1 institution in 1 country.

Hiroki MizukamiDepartment of Pathology and Molecular Medicine Hirosaki University Graduate School of Medicine Hirosaki Aomori Japan.
Kazunori TakahashiDepartment of Pathology and Molecular Medicine Hirosaki University Graduate School of Medicine Hirosaki Aomori Japan.
Wataru InabaDepartment of Pathology and Molecular Medicine Hirosaki University Graduate School of Medicine Hirosaki Aomori Japan.
Sho OsonoiDepartment of Pathology and Molecular Medicine Hirosaki University Graduate School of Medicine Hirosaki Aomori Japan.
Kosuke KamataDepartment of Pathology and Molecular Medicine Hirosaki University Graduate School of Medicine Hirosaki Aomori Japan.
Kentaro TsuboiDepartment of Pathology and Molecular Medicine Hirosaki University Graduate School of Medicine Hirosaki Aomori Japan.
Soroku YagihashiDepartment of Pathology and Molecular Medicine Hirosaki University Graduate School of Medicine Hirosaki Aomori Japan.
Hirosaki University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

AIMS/

introductionImpaired growth and premature death of β-cells are implicated in the progression of islet pathology in type 2 diabetes. It remains unclear, however, how aging affects islet cells, or whether the islet change in diabetes is an augmented process of aging. We studied age-related changes of the islet structure in Japanese non-diabetic subjects and explored the underlying mechanism of the changes. MATERIALS AND

methodsA total of 115 non-diabetic autopsy cases were subjected to morphometric analysis for volume densities of islets, β- and non-β-cells, as well as their masses. Proliferation activity identified by Ki67, and expressions of pancreatic and duodenal homeobox (PDX)-1, cell cycle inhibitor P16, and oxidative stress marker γH2AX were also examined.

resultsThere was a gradual and marginal decline of volume densities of islets, β- and non-β-cells with aging, while masses of these components were increased during maturation and slowly decreased after the 40s. Islet density was high in the young, but reduced after maturation. There was only a minimal influence of increased body mass index (BMI) on the increase in β-cell mass, but not on the other variables. Ki67 positivity and PDX-1 expressions were high in the young, but low after maturation, whereas expressions of P16 and γH2AX were elevated in the aged.

conclusionsAge-associated decline of β-cell mass is marginal after maturation, and the reduction of β-cell mass could be a specific process in diabetes. The impact of BMI on the islet structure is limited in Japanese with normal glucose tolerance.

Indexed as

AgingIslet structureβ‐Cell turnover

Identifiers

PMID24843735
PMCPMC4025233
OpenAlexW2014786199

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.