Evidence map›Paper›PMID 32070346›Full record

ArticleCardiovascular diabetology2020

Empagliflozin improved systolic blood pressure, endothelial dysfunction and heart remodeling in the metabolic syndrome ZSF1 rat.

Sin-Hee Park, Muhammad Akmal Farooq, Sébastien Gaertner, Christophe Bruckert, Abdul Wahid Qureshi, Hyun-Ho Lee, Djamel Benrahla, Brigitte Pollet, Dominique Stephan, Patrick Ohlmann and 5 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cardiovascular diabetology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
73citing papers in PubMed, 2 pooled it
11.4field-weighted citation impact, top 1% 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

73 citing papers in PubMed, 2 syntheses or guidelines pooled it, 124 citations in OpenAlex.

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13 more citing papers are in PubMed but not listed here.

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

15 authors at 5 institutions in 2 countries.

Sin-Hee ParkINSERM (French National Institute of Health and Medical Research), UMR 1260, Regenerative Nanomedicine, FMTS, Strasbourg, France.
Muhammad Akmal FarooqINSERM (French National Institute of Health and Medical Research), UMR 1260, Regenerative Nanomedicine, FMTS, Strasbourg, France.
Sébastien GaertnerINSERM (French National Institute of Health and Medical Research), UMR 1260, Regenerative Nanomedicine, FMTS, Strasbourg, France.
Christophe BruckertINSERM (French National Institute of Health and Medical Research), UMR 1260, Regenerative Nanomedicine, FMTS, Strasbourg, France.
Abdul Wahid QureshiINSERM (French National Institute of Health and Medical Research), UMR 1260, Regenerative Nanomedicine, FMTS, Strasbourg, France.
Hyun-Ho LeeINSERM (French National Institute of Health and Medical Research), UMR 1260, Regenerative Nanomedicine, FMTS, Strasbourg, France.
Djamel BenrahlaINSERM (French National Institute of Health and Medical Research), UMR 1260, Regenerative Nanomedicine, FMTS, Strasbourg, France.
Brigitte PolletUMR CNRS 7021 Laboratoire de Bioimagerie et Pathologies, Strasbourg, France.
Dominique StephanINSERM (French National Institute of Health and Medical Research), UMR 1260, Regenerative Nanomedicine, FMTS, Strasbourg, France.
Patrick OhlmannHôpitaux Universitaires de Strasbourg, Service de Cardiologie, Strasbourg, France.
Jean-Marc LessingerLaboratory of Biochemistry and Molecular Biology, Hôpitaux Universitaires de Strasbourg, Strasbourg, France.
Eric MayouxBoehringer Ingelheim Pharma GmbH & Co. KG, Biberach, Germany.
Cyril AugerINSERM (French National Institute of Health and Medical Research), UMR 1260, Regenerative Nanomedicine, FMTS, Strasbourg, France.
Olivier MorelINSERM (French National Institute of Health and Medical Research), UMR 1260, Regenerative Nanomedicine, FMTS, Strasbourg, France.
Valérie B Schini-KerthINSERM (French National Institute of Health and Medical Research), UMR 1260, Regenerative Nanomedicine, FMTS, Strasbourg, France. valerie.schini-kerth@unistra.fr.
Inserm · FRRegenerative NanoMedicine · FRHôpitaux Universitaires de Strasbourg · FRBoehringer Ingelheim (Germany) · DELaboratoire de Biophotonique et Pharmacologie · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundEmpagliflozin (empa), a selective sodium-glucose cotransporter (SGLT)2 inhibitor, reduced cardiovascular mortality and hospitalization for heart failure in patients with type 2 diabetes at high cardiovascular risk independent of glycemic control. The cardiovascular protective effect of empa was evaluated in an experimental model of metabolic syndrome, the obese ZSF1 rat, and its' lean control.

methodsLean and obese ZSF1 rats were either non-treated or treated with empa (30 mg/kg/day) for 6 weeks. Vascular reactivity was assessed using mesenteric artery rings, systolic blood pressure by tail-cuff sphygmomanometry, heart function and structural changes by echocardiography, and protein expression levels by Western blot analysis.

resultsEmpa treatment reduced blood glucose levels from 275 to 196 mg/dl in obese ZSF1 rats whereas normoglycemia (134 mg/dl) was present in control lean ZSF1 rats and was unaffected by empa. Obese ZSF1 rats showed increased systolic blood pressure, and blunted endothelium-dependent relaxations associated with the appearance of endothelium-dependent contractile responses (EDCFs) compared to control lean rats. These effects were prevented by the empa treatment. Obese ZSF1 rats showed increased weight of the heart and of the left ventricle volume without the presence of diastolic or systolic dysfunction, which were improved by the empa treatment. An increased expression level of senescence markers (p53, p21, p16), tissue factor, VCAM-1, SGLT1 and SGLT2 and a down-regulation of eNOS were observed in the aortic inner curvature compared to the outer one in the control lean rats, which were prevented by the empa treatment. In the obese ZSF1 rats, no such effects were observed. The empa treatment reduced the increased body weight and weight of lungs, spleen, liver and perirenal fat, hyperglycemia and the increased levels of total cholesterol and triglycerides in obese ZSF1 rats, and increased blood ketone levels and urinary glucose excretion in control lean and obese ZSF1 rats.

conclusionEmpa reduced glucose levels by 28% and improved both endothelial function and cardiac remodeling in the obese ZSF1 rat. Empa also reduced the increased expression level of senescence, and atherothrombotic markers at arterial sites at risk in the control lean, but not obese, ZSF1 rat.

Indexed as

AnimalsBenzhydryl CompoundsBiomarkersBlood GlucoseBlood PressureCellular SenescenceDisease Models, AnimalEndothelium, VascularGlucosidesMetabolic SyndromeObesityRats, ZuckerSodium-Glucose Transporter 2 InhibitorsSystoleVentricular Function, LeftVentricular RemodelingBenzhydryl CompoundsBiomarkersBlood GlucoseempagliflozinGlucosidesSodium-Glucose Transporter 2 InhibitorsEmpagliflozinEndothelial functionHeart functionHeart structureMetabolic syndromeSenescenceSGLT2ZSF1

Identifiers

PMID32070346
PMCPMC7026972
OpenAlexW3007147005

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Registered trials

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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.