Evidence map›Paper›PMID 26098416›Full record

ArticlePloS one2015

Impaired Coronary and Renal Vascular Function in Spontaneously Type 2 Diabetic Leptin-Deficient Mice.

Helena U Westergren, Julia Grönros, Suvi E Heinonen, Tasso Miliotis, Karin Jennbacken, Alan Sabirsh, Anette Ericsson, Ann-Cathrine Jönsson-Rylander, Sara Svedlund, Li-Ming Gan

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.5field-weighted citation impact, top 17% 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

18 citing papers in PubMed, 26 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Endothelial cell dysfunction in cardiac disease: driver or consequence?Frontiers in cell and developmental biology · 2023
    Review
  7. Article
  8. Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Review
  14. Design of Selective sPLAACS medicinal chemistry letters · 2018
    Article
  15. Article
  16. Ultrasonographic Characterization of theJournal of diabetes research · 2018
    Article
  17. Article
  18. Article
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 at 3 institutions in 1 country.

Helena U WestergrenDepartment of Molecular and Clinical Medicine, Institute of Medicine, Sahlgrenska Academy at the University of Gothenburg, Gothenburg, Sweden.
Julia GrönrosCVMD iMED, AstraZeneca R&D Mölndal, Mölndal, Sweden.
Suvi E HeinonenCVMD iMED, AstraZeneca R&D Mölndal, Mölndal, Sweden.
Tasso MiliotisCVMD iMED, AstraZeneca R&D Mölndal, Mölndal, Sweden.
Karin JennbackenCVMD iMED, AstraZeneca R&D Mölndal, Mölndal, Sweden.
Alan SabirshCVMD iMED, AstraZeneca R&D Mölndal, Mölndal, Sweden.
Anette EricssonCVMD iMED, AstraZeneca R&D Mölndal, Mölndal, Sweden.
Ann-Cathrine Jönsson-RylanderCVMD iMED, AstraZeneca R&D Mölndal, Mölndal, Sweden.
Sara SvedlundDepartment of Clinical Physiology, Sahlgrenska University Hospital, Gothenburg, Sweden.
Li-Ming GanDepartment of Molecular and Clinical Medicine, Institute of Medicine, Sahlgrenska Academy at the University of Gothenburg, Gothenburg, Sweden; CVMD iMED, AstraZeneca R&D Mölndal, Mölndal, Sweden; Department of Clinical Physiology, Sahlgrenska University Hospital, Gothenburg, Sweden.
AstraZeneca (Sweden) · SESahlgrenska University Hospital · SEUniversity of Gothenburg · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundType 2 diabetes is associated with macro- and microvascular complications in man. Microvascular dysfunction affects both cardiac and renal function and is now recognized as a main driver of cardiovascular mortality and morbidity. However, progression of microvascular dysfunction in experimental models is often obscured by macrovascular pathology and consequently demanding to study. The obese type 2 diabetic leptin-deficient (ob/ob) mouse lacks macrovascular complications, i.e. occlusive atherosclerotic disease, and may therefore be a potential model for microvascular dysfunction. The present study aimed to test the hypothesis that these mice with an insulin resistant phenotype might display microvascular dysfunction in both coronary and renal vascular beds. METHODS AND

resultsIn this study we used non-invasive Doppler ultrasound imaging to characterize microvascular dysfunction during the progression of diabetes in ob/ob mice. Impaired coronary flow velocity reserve was observed in the ob/ob mice at 16 and 21 weeks of age compared to lean controls. In addition, renal resistivity index as well as pulsatility index was higher in the ob/ob mice at 21 weeks compared to lean controls. Moreover, plasma L-arginine was lower in ob/ob mice, while asymmetric dimethylarginine was unaltered. Furthermore, a decrease in renal vascular density was observed in the ob/ob mice.

conclusionIn parallel to previously described metabolic disturbances, the leptin-deficient ob/ob mice also display cardiac and renal microvascular dysfunction. This model may therefore be suitable for translational, mechanistic and interventional studies to improve the understanding of microvascular complications in type 2 diabetes.

Indexed as

Coronary CirculationRenal CirculationAnimalsDiabetes Mellitus, Type 2Laser-Doppler FlowmetryLeptinMaleMiceUltrasonographyLeptin

Identifiers

PMID26098416
PMCPMC4476758
OpenAlexW813296191

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.