Evidence map›Paper›PMID 32999208›Full record

ArticleJournal of atherosclerosis and thrombosis2021

Glycation of HDL Polymerizes Apolipoprotein M and Attenuates Its Capacity to Bind to Sphingosine 1-Phosphate.

Tamaki Kobayashi, Makoto Kurano, Mai Nanya, Tomo Shimizu, Ryunosuke Ohkawa, Minoru Tozuka, Yutaka Yatomi

Open access · diamondAbstract read
In one paragraph

Article in Journal of atherosclerosis and thrombosis, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.4field-weighted citation impact, top 18% 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

17 citing papers in PubMed, 23 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. HDL metabolism and function in diabetes mellitus.Nature reviews. Endocrinology · 2026
    Review
  7. Review
  8. Observational
  9. Review
  10. Circulating Sphingolipids and Glucose Homeostasis: An Update.International journal of molecular sciences · 2023
    Review
  11. Article
  12. Review
  13. Article
  14. HDL Composition, Heart Failure, and Its Comorbidities.Frontiers in cardiovascular medicine · 2022
    Review
  15. Review
  16. Review
  17. 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

7 authors at 3 institutions in 1 country.

Tamaki KobayashiDepartment of Clinical Laboratory Medicine, The University of Tokyo.
Makoto KuranoDepartment of Clinical Laboratory Medicine, The University of Tokyo.
Mai NanyaDepartment of Clinical Laboratory Medicine, The University of Tokyo.
Tomo ShimizuResearch and Development Division, Tsukuba Research Institute, Sekisui Medical Co., Ltd.
Ryunosuke OhkawaAnalytical Laboratory Chemistry, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University.
Minoru TozukaLife Science Research Center, Nagano Children's Hospital.
Yutaka YatomiDepartment of Clinical Laboratory Medicine, The University of Tokyo.
The University of Tokyo · JPTokyo Medical and Dental University · JPNagano Children's Hospital · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimRecently, it has been established that most of the pleiotropic effects of high-density lipoprotein (HDL) are attributed to sphingosine 1-phosphate (S1P), which rides on HDL via apolipoprotein M (ApoM). In subjects with diabetes mellitus, both the pleiotropic effects of HDL and its role in reverse cholesterol transport are reported to be impaired. To elucidate the mechanisms underlying the impaired pleiotropic effects of HDL in subjects with diabetes, from the aspects of S1P and ApoM.

methodsThe incubation of HDL in a high-glucose condition resulted in the dimerization of ApoM. Moreover, the treatment of HDL with methylglyoxal resulted in the modulation of the ApoM structure, as suggested by the results of western blot analysis, isoelectric focusing electrophoresis, and two-dimensional gel electrophoresis, which was reversed by treatment with anti-glycation reagents.

resultsThe glycation of HDL resulted in impaired binding of the glycated HDL to S1P, and the S1P on glycated HDL degraded faster. In the case of human subjects, on the other hand, although both the serum ApoM levels and the ApoM content in HDL were lower in subjects with diabetes, we did not observe the polymerization of ApoM.

conclusionsModulation of the quantity and quality of ApoM might explain, at least in part, the impaired functions of HDL in subjects with diabetes mellitus. ApoM might be a useful target for laboratory testing and/or the treatment of diabetes mellitus.

Indexed as

Diabetes MellitusApolipoproteins MBiological TransportDrug DiscoveryElectrophoresis, Gel, Two-DimensionalGlycated ProteinsHumansIsoelectric FocusingLipoproteins, HDLLysophospholipidsSphingosineApolipoproteins Mglycated lipoproteins, HDLGlycated ProteinsLipoproteins, HDLLysophospholipidsSphingosinesphingosine 1-phosphateApolipoprotein MGlycationHDLSphingosine 1-phosphate

Identifiers

PMID32999208
PMCPMC8265924
OpenAlexW3090891574

What OpenQuestion holds

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LicenceCC BY-NC-SA
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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.