Evidence map›Paper›PMID 36277717›Full record

ArticleFrontiers in endocrinology2022

Alpha cell dysfunction in type 1 diabetes is independent of a senescence program.

Gabriel Brawerman, Vasilis Ntranos, Peter J Thompson

Open access · goldAbstract read
In one paragraph

Article in Frontiers in endocrinology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
3.9field-weighted citation impact, top 6% 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

18 citing papers in PubMed, 19 citations in OpenAlex.

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  17. The human α cell in health and disease.The Journal of endocrinology · 2023
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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

3 authors at 3 institutions in 2 countries.

Gabriel BrawermanDepartment of Physiology & Pathophysiology, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, MB, Canada.
Vasilis NtranosDepartment of Epidemiology and Biostatistics, University of California San Francisco, San Francisco, CA, United States.
Peter J ThompsonDepartment of Physiology & Pathophysiology, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, MB, Canada.
Children's Hospital Research Institute of Manitoba · CAUniversity of California, San Francisco · USUniversity of Manitoba · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Type 1 Diabetes (T1D) is caused by insulin deficiency, due to progressive autoimmune destruction of pancreatic β cells. Glucagon-secreting α cells become dysfunctional in T1D and contribute to pathophysiology, however, the mechanisms involved are unclear. While the majority of β cells are destroyed in T1D, some β cells escape this fate and become senescent but whether α cell dysfunction involves a senescence program has not been explored. Here we addressed the question of whether α cells become senescent during the natural history of T1D in the non-obese diabetic (NOD) mouse model and humans. NOD mice had several distinct subpopulations of α cells, but none were defined by markers of senescence at the transcriptional or protein level. Similarly, α cells of human T1D donors did not express senescence markers. Despite the lack of senescence in α cells

Indexed as

Diabetes Mellitus, Type 1Glucagon-Secreting CellsAnimalsBiomarkersGlucagonHumansInsulinMiceMice, Inbred NODBiomarkersGlucagonInsulinalpha cells of pancreatic isletDNA damage response (DDR)glucagon secretionsenescenceType 1 diabetes (T1D)

Identifiers

PMID36277717
PMCPMC9586489
OpenAlexW4303183085

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.