Evidence map›Paper›PMID 39037711›Full record

ArticleClinical science (London, England : 1979)2024

Differences in endothelial function between patients with Type 1 and Type 2 diabetes: effects of red blood cells and arginase.

John Tengbom, Eftychia Kontidou, Aida Collado, Jiangning Yang, Michael Alvarsson, Jonas Brinck, Sophia Rössner, Zhichao Zhou, John Pernow, Ali Mahdi

Abstract readComparative Study
In one paragraph

Article in Clinical science (London, England : 1979), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
–field-weighted citation impact
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

4 citing papers in PubMed.

  1. Trial
  2. Review
  3. Article
  4. 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

10 authors.

John TengbomDivision of Cardiology, Department of Medicine Solna, Karolinska Institutet, Karolinska University Hospital, Stockholm, Sweden.ORCID 0000-0003-3608-160X
Eftychia KontidouDivision of Cardiology, Department of Medicine Solna, Karolinska Institutet, Karolinska University Hospital, Stockholm, Sweden.
Aida ColladoDivision of Cardiology, Department of Medicine Solna, Karolinska Institutet, Karolinska University Hospital, Stockholm, Sweden.
Jiangning YangDivision of Cardiology, Department of Medicine Solna, Karolinska Institutet, Karolinska University Hospital, Stockholm, Sweden.
Michael AlvarssonDivision of Endocrinology and Diabetology, Department of Molecular Medicine and Surgery, Karolinska Institutet, Karolinska University Hospital, Stockholm, Sweden.
Jonas BrinckDivision of Endocrinology, Department of Medicine Huddinge, Karolinska Institutet, Karolinska University Hospital, Stockholm, Sweden.
Sophia RössnerDivision of Endocrinology, Department of Medicine Huddinge, Karolinska Institutet, Karolinska University Hospital, Stockholm, Sweden.
Zhichao ZhouDivision of Cardiology, Department of Medicine Solna, Karolinska Institutet, Karolinska University Hospital, Stockholm, Sweden.
John Pernow *Division of Cardiology, Department of Medicine Solna, Karolinska Institutet, Karolinska University Hospital, Stockholm, Sweden.
Ali Mahdi *Division of Cardiology, Department of Medicine Solna, Karolinska Institutet, Karolinska University Hospital, Stockholm, Sweden.

Funding

EFSD/Novo Nordisk Foundation Future Leaders Award NNF22SA0081227Foundation for Geriatric Diseases 2023-01860Hjärt-Lungfonden (Swedish Heart-Lung Foundation) 20190266Hjärt-Lungfonden (Swedish Heart-Lung Foundation) 20200326Hjärt-Lungfonden (Swedish Heart-Lung Foundation) 20220210Hjärt-Lungfonden (Swedish Heart-Lung Foundation) 20220264Hjärt-Lungfonden (Swedish Heart-Lung Foundation) 20230386Hjärt-Lungfonden (Swedish Heart-Lung Foundation) 20240072Swedish Research Council 2020-01372Swedish Research Council 2023-02508
6 · The paper itself

Abstract

The mechanisms underlying endothelial dysfunction in Type 1 and Type 2 diabetes (T1DM and T2DM) are unresolved. The red blood cells (RBCs) with increased arginase activity induce endothelial dysfunction in T2DM, but the implications of RBCs and the role of arginase inhibition in T1DM are unexplored. We aimed to investigate the differences in endothelial function in patients with T1DM and T2DM, with focus on RBCs and arginase. Thirteen patients with T1DM and twenty-six patients with T2DM, matched for HbA1c and sex were included. In vivo endothelium-dependent and -independent vasodilation (EDV and EIDV) were assessed by venous occlusion plethysmography before and after administration of an arginase inhibitor. RBCs were co-incubated with rat aortic segments for 18h followed by evaluation of endothelium-dependent (EDR) and -independent relaxation (EIDR) in isolated organ chambers. In vivo EDV, but not EIDV, was significantly impaired in patients with T2DM compared with patients with T1DM. Arginase inhibition resulted in improved EDV only in T2DM. RBCs from patients with T2DM induced impaired EDR but not EIDR in isolated aortic segments, whereas RBCs from patients with T1DM did not affect EDR nor EIDR. The present study demonstrates markedly impaired EDV in patients with T2DM in comparison with T1DM. In addition, it highlights the divergent roles of RBCs and arginase in mediating endothelial dysfunction in T1DM and T2DM. While endothelial dysfunction is mediated via RBCs and arginase in T2DM, these phenomena are not prominent in T1DM thereby indicating distinct differences in underlying mechanisms.

Indexed as

ArginaseDiabetes Mellitus, Type 1Diabetes Mellitus, Type 2Endothelium, VascularErythrocytesVasodilationAdultAgedAnimalsAortaEnzyme InhibitorsFemaleHumansMaleMiddle AgedArginaseEnzyme Inhibitorsarginasediabetes mellitusendothelial dysfunctionred blood cells

Identifiers

PMID39037711
PMCPMC11300671

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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.