Evidence map›Paper›PMID 28410399›Full record

ArticlePloS one2017

Altered glucose metabolism and hypoxic response in alloxan-induced diabetic atherosclerosis in rabbits.

Yunosuke Matsuura, Atsushi Yamashita, Yan Zhao, Takashi Iwakiri, Kazuaki Yamasaki, Chihiro Sugita, Chihiro Koshimoto, Kazuo Kitamura, Keiichi Kawai, Nagara Tamaki and 3 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.1field-weighted citation impact, top 23% 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

9 citing papers in PubMed, 18 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Role of glycolysis in diabetic atherosclerosis.World journal of diabetes · 2023
    Review
  5. Article
  6. Article
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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

13 authors at 5 institutions in 1 country.

Yunosuke MatsuuraDepartment of Pathology, Faculty of Medicine, University of Miyazaki, Miyazaki, Japan.
Atsushi YamashitaDepartment of Pathology, Faculty of Medicine, University of Miyazaki, Miyazaki, Japan.ORCID http://orcid.org/0000-0001-5487-7594
Yan ZhaoDepartment of Tracer Kinetics and Bioanalysis, Graduate School of Medicine, Hokkaido University, Sapporo, Japan.
Takashi IwakiriDepartment of Pathology, Faculty of Medicine, University of Miyazaki, Miyazaki, Japan.
Kazuaki YamasakiDepartment of Tracer Kinetics and Bioanalysis, Graduate School of Medicine, Hokkaido University, Sapporo, Japan.
Chihiro SugitaDepartment of Pathology, Faculty of Medicine, University of Miyazaki, Miyazaki, Japan.
Chihiro KoshimotoFrontier Science Research Center, University of Miyazaki, Miyazaki, Japan.
Kazuo KitamuraDepartment of Internal Medicine, Faculty of Medicine, University of Miyazaki, Miyazaki, Japan.
Keiichi KawaiFaculty of Health Sciences, Institute of Medical, Pharmaceutical and Health Sciences, Kanazawa University, Kanazawa, Japan.
Nagara TamakiDepartment of Nuclear Medicine, Graduate School of Medicine, Hokkaido University, Sapporo, Japan.
Songji ZhaoDepartment of Tracer Kinetics and Bioanalysis, Graduate School of Medicine, Hokkaido University, Sapporo, Japan.
Yuji KugeDepartment of Integrated Molecular Imaging, Graduate School of Medicine, Hokkaido University, Sapporo, Japan.
Yujiro AsadaDepartment of Pathology, Faculty of Medicine, University of Miyazaki, Miyazaki, Japan.
University of Miyazaki · JPHokkaido University · JPHokkaido University of Science · JPKanazawa University · JPKyushu University of Health and Welfare · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Diabetes mellitus accelerates atherosclerosis that causes most cardiovascular events. Several metabolic pathways are considered to contribute to the development of atherosclerosis, but comprehensive metabolic alterations to atherosclerotic arterial cells remain unknown. The present study investigated metabolic changes and their relationship to vascular histopathological changes in the atherosclerotic arteries of rabbits with alloxan-induced diabetes. Diabetic atherosclerosis was induced in rabbit ilio-femoral arteries by injecting alloxan (100 mg/kg), injuring the arteries using a balloon, and feeding with a 0.5% cholesterol diet. We histologically assessed the atherosclerotic lesion development, cellular content, pimonidazole positive-hypoxic area, the nuclear localization of hypoxia-inducible factor-1α, and apoptosis. We evaluated comprehensive arterial metabolism by performing metabolomic analyses using capillary electrophoresis-time of flight mass spectrometry. We evaluated glucose uptake and its relationship to vascular hypoxia using 18F-fluorodeoxyglucose and pimonidazole. Plaque burden, macrophage content, and hypoxic areas were more prevalent in arteries with diabetic, than non-diabetic atherosclerosis. Metabolomic analyses highlighted 12 metabolites that were significantly altered between diabetic and non-diabetic atherosclerosis. A half of them were associated with glycolysis metabolites, and their levels were decreased in diabetic atherosclerosis. The uptake of glucose evaluated as 18F-fluorodeoxyglucose in atherosclerotic lesions increased according to increased macrophage content or hypoxic areas in non-diabetic, but not diabetic rabbits. Despite profound hypoxic areas, the nuclear localization of hypoxia-inducible factor-1α decreased and the number of apoptotic cells increased in diabetic atherosclerotic lesions. Altered glycolysis metabolism and an impaired response to hypoxia in atherosclerotic lesions under conditions of insulin-dependent diabetes might be involved in the development of diabetic atherosclerosis.

Indexed as

HypoxiaAlloxanAnimalsApoptosisAtherosclerosisAutoradiographyBody WeightCluster AnalysisDiabetes Mellitus, ExperimentalDiet, High-FatElectrophoresis, CapillaryFemoral ArteryFluorodeoxyglucose F18GlucoseGlycolysisHypoxia-Inducible Factor 1, alpha SubunitAlloxanFluorodeoxyglucose F18GlucoseHypoxia-Inducible Factor 1, alpha SubunitNitroimidazolespimonidazole

Identifiers

PMID28410399
PMCPMC5391952
OpenAlexW2606896242

What OpenQuestion holds

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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.