Evidence map›Paper›PMID 36139067›Full record

ReviewBiomolecules2022

Role of Reactive Oxygen Species in Glucose Metabolism Disorder in Diabetic Pancreatic β-Cells.

Eri Mukai, Shimpei Fujimoto, Nobuya Inagaki

Open access · goldAbstract readReview
In one paragraph

Review in Biomolecules, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed, 2 pooled it
11.6field-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

37 citing papers in PubMed, 2 syntheses or guidelines pooled it, 59 citations in OpenAlex.

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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 1 country.

Eri MukaiMedical Physiology and Metabolism Laboratory, Department of Biomedical Sciences, College of Life Sciences, Ritsumeikan University, Kusatsu 5258577, Japan.
Shimpei FujimotoDepartment of Endocrinology, Metabolism, and Nephrology, Kochi Medical School, Kochi University, Kochi 7838505, Japan.
Nobuya InagakiDepartment of Diabetes, Endocrinology and Nutrition, Graduate School of Medicine, Kyoto University, Kyoto 6068507, Japan.ORCID 0000-0001-8261-2593
Kōchi University · JPKyoto University · JPRitsumeikan University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The dysfunction of pancreatic β-cells plays a central role in the onset and progression of type 2 diabetes mellitus (T2DM). Insulin secretory defects in β-cells are characterized by a selective impairment of glucose stimulation, and a reduction in glucose-induced ATP production, which is essential for insulin secretion. High glucose metabolism for insulin secretion generates reactive oxygen species (ROS) in mitochondria. In addition, the expression of antioxidant enzymes is very low in β-cells. Therefore, β-cells are easily exposed to oxidative stress. In islet studies using a nonobese T2DM animal model that exhibits selective impairment of glucose-induced insulin secretion (GSIS), quenching ROS generated by glucose stimulation and accumulated under glucose toxicity can improve impaired GSIS. Acute ROS generation and toxicity cause glucose metabolism disorders through different molecular mechanisms. Nuclear factor erythroid 2-related factor 2 (Nrf2), a transcription factor, is a master regulator of antioxidant defense and a potential therapeutic target in oxidative stress-related diseases, suggesting the possible involvement of Nrf2 in β-cell dysfunction caused by ROS. In this review, we describe the mechanisms of insulin secretory defects induced by oxidative stress in diabetic β-cells.

Indexed as

Diabetes Mellitus, Type 2Insulin-Secreting CellsAdenosine TriphosphateAnimalsAntioxidantsGlucoseInsulinNF-E2-Related Factor 2Oxidative StressReactive Oxygen SpeciesAdenosine TriphosphateAntioxidantsGlucoseInsulinNF-E2-Related Factor 2Reactive Oxygen Speciesglucose metabolisminsulin secretionoxidative stresspancreatic β-cellsreactive oxygen species

Identifiers

PMID36139067
PMCPMC9496160
OpenAlexW4294989688

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.