Evidence map›Paper›PMID 31915150›Full record

ArticleDiabetes2020

Protection Against Insulin Resistance by Apolipoprotein M/Sphingosine-1-Phosphate.

Makoto Kurano, Kazuhisa Tsukamoto, Tomo Shimizu, Hidetoshi Kassai, Kazuki Nakao, Atsu Aiba, Masumi Hara, Yutaka Yatomi

Abstract read
PubMed Publisher
In one paragraph

Article in Diabetes, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed, 1 pooled it
4.2field-weighted citation impact, top 5% 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

48 citing papers in PubMed, 1 synthesis or guideline pooled it, 71 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. Review
  6. Article
  7. Review
  8. Article
  9. Observational
  10. Review
  11. Article
  12. Review
  13. Sphingosine 1-Phosphate Regulates Obesity and Glucose Homeostasis.International journal of molecular sciences · 2024
    Review
  14. Review
  15. Circulating Sphingolipids and Glucose Homeostasis: An Update.International journal of molecular sciences · 2023
    Review
  16. Review
  17. Review
  18. Article
  19. Article
  20. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 4 institutions in 1 country.

Makoto KuranoDepartment of Clinical Laboratory Medicine, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan kurano-tky@umin.ac.jp yatoyuta-tky@umin.ac.jp.ORCID 0000-0002-2596-1145
Kazuhisa TsukamotoDepartment of Internal Medicine, Teikyo University School of Medicine, Tokyo, Japan.
Tomo ShimizuResearch & Development Division, Tsukuba Research Institute, Sekisui Medical Co., Ltd., Ibaraki, Japan.
Hidetoshi KassaiLaboratory of Animal Resources, Center for Disease Biology and Integrative Medicine, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Kazuki NakaoLaboratory of Animal Resources, Center for Disease Biology and Integrative Medicine, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Atsu AibaLaboratory of Animal Resources, Center for Disease Biology and Integrative Medicine, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Masumi HaraDepartment of Internal Medicine, Mizonokuchi Hospital, Teikyo University School of Medicine, Kanagawa, Japan.
Yutaka YatomiDepartment of Clinical Laboratory Medicine, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan kurano-tky@umin.ac.jp yatoyuta-tky@umin.ac.jp.ORCID 0000-0003-1719-4297
The University of Tokyo · JPFukushima Medical University · JPSekisui Medical (Japan) · JPTeikyo University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Subjects with low serum HDL cholesterol levels are reported to be susceptible to diabetes, with insulin resistance believed to be the underlying pathological mechanism. Apolipoprotein M (apoM) is a carrier of sphingosine-1-phosphate (S1P), a multifunctional lipid mediator, on HDL, and the pleiotropic effects of HDL are believed to be mediated by S1P. In the current study, we attempted to investigate the potential association between apoM/S1P and insulin resistance. We observed that the serum levels of apoM were lower in patients with type 2 diabetes and that they were negatively correlated with BMI and the insulin resistance index. While deletion of apoM in mice was associated with worsening of insulin resistance, overexpression of apoM was associated with improvement of insulin resistance. Presumably, apoM/S1P exerts its protective effect against insulin resistance by activating insulin signaling pathways, such as the AKT and AMPK pathways, and also by improving the mitochondrial functions through upregulation of SIRT1 protein levels. These actions of apoM/S1P appear to be mediated via activation of S1P1 and/or S1P3. These results suggest that apoM/S1P exerts protective roles against the development of insulin resistance.

Indexed as

Insulin ResistanceAdultAnimalsApolipoproteins MBlood GlucoseBody Mass IndexDiabetes Mellitus, Type 2Dietary FatsDiet, High-FatFemaleGene Expression RegulationGlycated HemoglobinHep G2 CellsHumansLipid MetabolismLipidsApolipoproteins MAPOM protein, humanApoM protein, mouseBlood GlucoseDietary FatsGlycated HemoglobinLipidsLysophospholipidsSphingosinesphingosine 1-phosphate

Identifiers

PMID31915150
OpenAlexW2999812614

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.