Evidence map›Paper›PMID 30447687›Full record

ArticleCardiovascular diabetology2018

A SGLT2 inhibitor dapagliflozin suppresses prolonged ventricular-repolarization through augmentation of mitochondrial function in insulin-resistant metabolic syndrome rats.

Aysegul Durak, Yusuf Olgar, Sinan Degirmenci, Erman Akkus, Erkan Tuncay, Belma Turan

Open access · goldAbstract readComparative Study
In one paragraph

Article in Cardiovascular diabetology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 93 papers.

0numbers the graph read from it
0cells of the map it votes in
93citing papers in PubMed
16.1field-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

93 citing papers in PubMed, 171 citations in OpenAlex.

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  14. The use of SGLT2 inhibitors in older people: What is important?Aging clinical and experimental research · 2025
    Review
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  19. SGLT2 inhibitors: how do they affect the cardiac cells.Molecular and cellular biochemistry · 2025
    Review
  20. Energy metabolism in health and diseases.Signal transduction and targeted therapy · 2025
    Review

33 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

6 authors at 1 institution in 1 country.

Aysegul DurakDepartments of Biophysics, Faculty of Medicine, Ankara University, Ankara, Turkey.
Yusuf OlgarDepartments of Biophysics, Faculty of Medicine, Ankara University, Ankara, Turkey.
Sinan DegirmenciDepartments of Biophysics, Faculty of Medicine, Ankara University, Ankara, Turkey.
Erman AkkusInternal Medicine, Faculty of Medicine, Ankara University, Ankara, Turkey.
Erkan TuncayDepartments of Biophysics, Faculty of Medicine, Ankara University, Ankara, Turkey.
Belma TuranDepartments of Biophysics, Faculty of Medicine, Ankara University, Ankara, Turkey. belma.turan@medicine.ankara.edu.tr.
Ankara University · TR

Funding

TUBITAK SBAG-214S254
6 · The paper itself

Abstract

backgroundMetabolic syndrome (MetS) is a prevalent risk factor for cardiac dysfunction. Although SGLT2-inhibitors have important cardioprotective effects in hyperglycemia, their underlying mechanisms are complex and not completely understood. Therefore, we examined mechanisms of a SGLT2-inhibitor dapagliflozin (DAPA)-related cardioprotection in overweight insulin-resistant MetS-rats comparison with insulin (INSU), behind its glucose-lowering effect.

methodsA 28-week high-carbohydrate diet-induced MetS-rats received DAPA (5 mg/kg), INSU (0.15 mg/kg) or vehicle for 2 weeks. To validate MetS-induction, we monitored all animals weekly by measuring body weight, blood glucose and HOMO-IR index, electrocardiograms, heart rate, systolic and diastolic pressures.

resultsDAPA-treatment of MetS-rats significantly augmented the increased blood pressure, prolonged Q-R interval, and low heart rate with depressed left ventricular function and relaxation of the aorta. Prolonged-action potentials were preserved with DAPA-treatment, more prominently than INSU-treatment, at most, through the augmentation in depressed voltage-gated K

conclusionsOverall, our data provided a new insight into DAPA-associated cardioprotection in MetS rats, including suppression of prolonged ventricular-repolarization through augmentation of mitochondrial function and oxidative stress followed by improvement of fusion-fission proteins, out of its glucose-lowering effect.

Indexed as

Insulin ResistanceAction PotentialsAnimalsArrhythmias, CardiacBenzhydryl CompoundsBlood GlucoseDisease Models, AnimalGlucosidesHeart RateHeart VentriclesInsulinMaleMembrane Potential, MitochondrialMetabolic SyndromeMitochondria, HeartMyocytes, CardiacBenzhydryl CompoundsBlood GlucosedapagliflozinGlucosidesInsulinPotassium Channels, Voltage-GatedSlc5a2 protein, ratSodium-Glucose Transporter 2Sodium-Glucose Transporter 2 InhibitorsVoltage-Gated Sodium ChannelsDiabetesElectrophysiologyHeart functionInsulin resistanceOxidative stressSGLT2 inhibitors

Identifiers

PMID30447687
PMCPMC6240275
OpenAlexW2900665718

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.