Evidence map›Paper›PMID 27225690›Full record

ReviewAntioxidants & redox signaling2017

The Role of Oxidative Stress and Hypoxia in Pancreatic Beta-Cell Dysfunction in Diabetes Mellitus.

Philipp A Gerber, Guy A Rutter

Open access · hybridAbstract readReview
In one paragraph

Review in Antioxidants & redox signaling, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 292 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
292citing papers in PubMed, 4 pooled it
37.3field-weighted citation impact, top 1% 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

292 citing papers in PubMed, 4 syntheses or guidelines pooled it, 633 citations in OpenAlex.

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  3. The effect of ambient ozone exposure on three types of diabetes: a meta-analysis.Environmental health : a global access science source · 2023
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232 more citing papers are in PubMed but not listed here.

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

2 authors at 2 institutions in 2 countries.

Philipp A Gerber1 Department of Endocrinology, Diabetes and Clinical Nutrition, University Hospital Zurich , Zurich, Switzerland .
Guy A Rutter2 Section of Cell Biology and Functional Genomics, Department of Medicine, Imperial College London , London, United Kingdom .
Genomics England · GBUniversity Hospital of Zurich · CH

Funding

Biotechnology and Biological Sciences Research Council BB/J015873/1Medical Research Council MR/J0003042/1Medical Research Council MR/K001981/1Wellcome Trust WT098424AIA
6 · The paper itself

Abstract

significanceMetabolic syndrome is a frequent precursor of type 2 diabetes mellitus (T2D), a disease that currently affects ∼8% of the adult population worldwide. Pancreatic beta-cell dysfunction and loss are central to the disease process, although understanding of the underlying molecular mechanisms is still fragmentary. Recent Advances: Oversupply of nutrients, including glucose and fatty acids, and the subsequent overstimulation of beta cells, are believed to be an important contributor to insulin secretory failure in T2D. Hypoxia has also recently been implicated in beta-cell damage. Accumulating evidence points to a role for oxidative stress in both processes. Although the production of reactive oxygen species (ROS) results from enhanced mitochondrial respiration during stimulation with glucose and other fuels, the expression of antioxidant defense genes is unusually low (or disallowed) in beta cells. CRITICAL ISSUES: Not all subjects with metabolic syndrome and hyperglycemia go on to develop full-blown diabetes, implying an important role in disease risk for gene-environment interactions. Possession of common risk alleles at the SLC30A8 locus, encoding the beta-cell granule zinc transporter ZnT8, may affect cytosolic Zn FUTURE DIRECTIONS: Loss of normal beta-cell function, rather than total mass, is increasingly considered to be the major driver for impaired insulin secretion in diabetes. Better understanding of the role of oxidative changes, its modulation by genes involved in disease risk, and effects on beta-cell identity may facilitate the development of new therapeutic strategies to this disease. Antioxid. Redox Signal. 26, 501-518.

Indexed as

Oxidative StressAnimalsAntioxidantsDiabetes MellitusDiabetes Mellitus, Type 2GlucoseHumansHypoxiaInsulinInsulin-Secreting CellsIslets of LangerhansIslets of Langerhans TransplantationLipid MetabolismMitochondriaReactive Oxygen SpeciesZincAntioxidantsGlucoseInsulinReactive Oxygen SpeciesZincbeta celldiabeteshypoxiainsulin secretionzinc

Identifiers

PMID27225690
PMCPMC5372767
OpenAlexW2405977822

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.