Evidence map›Paper›PMID 29331666›Full record

ArticleRedox biology2018

Age-related oxidative changes in pancreatic islets are predominantly located in the vascular system.

Richard Kehm, Jeannette König, Kerstin Nowotny, Tobias Jung, Stephanie Deubel, Sabrina Gohlke, Tim Julius Schulz, Annika Höhn

Open access · goldAbstract read
In one paragraph

Article in Redox biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
0.7field-weighted citation impact, top 25% 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

23 citing papers in PubMed, 38 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. The mitochondrial enzyme pyruvate carboxylase restricts pancreatic β-cell senescence by blocking p53 activation.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Biomarkers of aging.Science China. Life sciences · 2023
    Review
  14. Changes in Pancreatic Senescence Mediate Pancreatic Diseases.International journal of molecular sciences · 2023
    Review
  15. Article
  16. Article
  17. Article
  18. Article
  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

8 authors at 3 institutions in 1 country.

Richard KehmDepartment of Molecular Toxicology, German Institute of Human Nutrition Potsdam-Rehbruecke (DIfE), 14558 Nuthetal, Germany; German Center for Diabetes Research (DZD), 85764 Muenchen-Neuherberg, Germany. Electronic address: richard.kehm@dife.de.
Jeannette KönigDepartment of Molecular Toxicology, German Institute of Human Nutrition Potsdam-Rehbruecke (DIfE), 14558 Nuthetal, Germany. Electronic address: jeannette.koenig@dife.de.
Kerstin NowotnyDepartment of Molecular Toxicology, German Institute of Human Nutrition Potsdam-Rehbruecke (DIfE), 14558 Nuthetal, Germany. Electronic address: kerstin.nowotny@dife.de.
Tobias JungDepartment of Molecular Toxicology, German Institute of Human Nutrition Potsdam-Rehbruecke (DIfE), 14558 Nuthetal, Germany. Electronic address: tobias.jung@dife.de.
Stephanie DeubelDepartment of Molecular Toxicology, German Institute of Human Nutrition Potsdam-Rehbruecke (DIfE), 14558 Nuthetal, Germany. Electronic address: stefanie.deubel@dife.de.
Sabrina GohlkeDepartment of Adipocyte Development and Nutrition, German Institute of Human Nutrition Potsdam-Rehbruecke (DIfE), 14558 Nuthetal, Germany; German Center for Diabetes Research (DZD), 85764 Muenchen-Neuherberg, Germany. Electronic address: sabrina.gohlke@dife.de.
Tim Julius SchulzDepartment of Adipocyte Development and Nutrition, German Institute of Human Nutrition Potsdam-Rehbruecke (DIfE), 14558 Nuthetal, Germany; German Center for Diabetes Research (DZD), 85764 Muenchen-Neuherberg, Germany. Electronic address: tim.schulz@dife.de.
Annika HöhnDepartment of Molecular Toxicology, German Institute of Human Nutrition Potsdam-Rehbruecke (DIfE), 14558 Nuthetal, Germany; German Center for Diabetes Research (DZD), 85764 Muenchen-Neuherberg, Germany. Electronic address: annika.hoehn@dife.de.
German Institute of Human Nutrition · DEDeutsches Diabetes-Zentrum e.V. · DEHeinrich Heine University Düsseldorf · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Aged tissues usually show a decreased regenerative capacity accompanied by a decline in functionality. During aging pancreatic islets also undergo several morphological and metabolic changes. Besides proliferative and regenerative limitations, endocrine cells lose their secretory capacity, contributing to a decline in functional islet mass and a deregulated glucose homeostasis. This is linked to several features of aging, such as induction of cellular senescence or the formation of modified proteins, such as advanced glycation end products (AGEs) - the latter mainly examined in relation to hyperglycemia and in disease models. However, age-related changes of endocrine islets under normoglycemic and non-pathologic conditions are poorly investigated. Therefore, a characterization of pancreatic tissue sections as wells as plasma samples of wild-type mice (C57BL/6J) at various age groups (2.5, 5, 10, 15, 21 months) was performed. Our findings reveal that mice at older age are able to secret sufficient amounts of insulin to maintain normoglycemia. During aging the pancreatic islet area increased and the islet size doubled in 21 months old mice when compared to 2.5 months old mice, whereas the islet number was unchanged. This was accompanied by an age-dependent decrease in Ki-67 levels and pancreatic duodenal homeobox-1 (PDX-1), indicating a decline in proliferative and regenerative capacity of pancreatic islets with advancing age. In contrast, the number of p16

Indexed as

AgingAnimalsBlood GlucoseGlucoseGlycation End Products, AdvancedHomeodomain ProteinsHomeostasisInsulinIslets of LangerhansKi-67 AntigenMiceNitric Oxide Synthase Type IIOxidative StressTrans-ActivatorsBlood GlucoseGlucoseGlycation End Products, AdvancedHomeodomain ProteinsInsulinKi-67 AntigenMki67 protein, mouseNitric Oxide Synthase Type IINOS2 protein, humanpancreatic and duodenal homeobox 1 proteinTrans-ActivatorsAdvanced glycation end productsAgingCellular senescencePancreatic islets

Identifiers

PMID29331666
PMCPMC5772008
OpenAlexW2778315707

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.