Evidence map›Paper›PMID 28086951›Full record

ArticleCardiovascular diabetology2017

Sodium glucose transporter 2 (SGLT2) inhibition with empagliflozin improves cardiac diastolic function in a female rodent model of diabetes.

Javad Habibi, Annayya R Aroor, James R Sowers, Guanghong Jia, Melvin R Hayden, Mona Garro, Brady Barron, Eric Mayoux, R Scott Rector, Adam Whaley-Connell and 1 more

Open access · goldAbstract read
In one paragraph

Article in Cardiovascular diabetology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 143 papers, 7 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
143citing papers in PubMed, 7 pooled it
19.0field-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

143 citing papers in PubMed, 7 syntheses or guidelines pooled it, 269 citations in OpenAlex.

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  19. SGLT2 inhibitors: how do they affect the cardiac cells.Molecular and cellular biochemistry · 2025
    Review
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83 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

11 authors at 3 institutions in 3 countries.

Javad HabibiDepartment of Medicine, Division of Endocrinology, Diabetes and Cardiovascular Center, University of Missouri, School of Medicine, Columbia, USA.
Annayya R AroorDepartment of Medicine, Division of Endocrinology, Diabetes and Cardiovascular Center, University of Missouri, School of Medicine, Columbia, USA.
James R SowersDepartment of Medicine, Division of Endocrinology, Diabetes and Cardiovascular Center, University of Missouri, School of Medicine, Columbia, USA.
Guanghong JiaDepartment of Medicine, Division of Endocrinology, Diabetes and Cardiovascular Center, University of Missouri, School of Medicine, Columbia, USA.
Melvin R HaydenDepartment of Medicine, Division of Endocrinology, Diabetes and Cardiovascular Center, University of Missouri, School of Medicine, Columbia, USA.
Mona GarroDepartment of Medicine, Division of Endocrinology, Diabetes and Cardiovascular Center, University of Missouri, School of Medicine, Columbia, USA.
Brady BarronDepartment of Medicine, Division of Endocrinology, Diabetes and Cardiovascular Center, University of Missouri, School of Medicine, Columbia, USA.
Eric MayouxDepartment of Cardiometabolic Diseases Research, Boehringer-Ingelheim, Biberach, Germany.
R Scott RectorResearch Service, Harry S. Truman Memorial Veterans Hospital, Columbia, MO, USA.
Adam Whaley-ConnellDepartment of Medicine, Division of Endocrinology, Diabetes and Cardiovascular Center, University of Missouri, School of Medicine, Columbia, USA.
Vincent G DeMarcoDepartment of Medicine, Division of Endocrinology, Diabetes and Cardiovascular Center, University of Missouri, School of Medicine, Columbia, USA. demarcov@missouri.edu.ORCID 0000-0003-2092-9995
Harry S. Truman Memorial Veterans' Hospital · USBoehringer Ingelheim (Germany) · DEUniversity of Missouri · US

Funding

Ang II and Overnutrition and Insulin resistance in Cardiovascular TissueR01HL107910 · NHLBI · UNIVERSITY OF MISSOURI-COLUMBIA · PI SOWERS, JAMES RUSSELL · 2011 to 2015
$1.8M
Hepatic Mitochondria and Insulin Resistance in Fatty Liver and Type 2 DiabetesIK2BX001299 · VA · HARRY S. TRUMAN MEMORIAL VA HOSPITAL · PI RECTOR, RANDY SCOTT · 2011 to 2015
–
BLRD VA IK2 BX001299NHLBI NIH HHS R01 HL107910
6 · The paper itself

Abstract

Obese and diabetic individuals are at increased risk for impairments in diastolic relaxation and heart failure with preserved ejection fraction. The impairments in diastolic relaxation are especially pronounced in obese and diabetic women and predict future cardiovascular disease (CVD) events in this population. Recent clinical data suggest sodium glucose transporter-2 (SGLT2) inhibition reduces CVD events in diabetic individuals, but the mechanisms of this CVD protection are unknown. To determine whether targeting SGLT2 improves diastolic relaxation, we utilized empagliflozin (EMPA) in female db/db mice. Eleven week old female db/db mice were fed normal mouse chow, with or without EMPA, for 5 weeks. Blood pressure (BP), HbA1c and fasting glucose were significantly increased in untreated db/db mice (DbC) (P < 0.01). EMPA treatment (DbE) improved glycemic indices (P < 0.05), but not BP (P > 0.05). At baseline, DbC and DbE had already established impaired diastolic relaxation as indicated by impaired septal wall motion (>tissue Doppler derived E'/A' ratio) and increased left ventricular (LV) filling pressure (<E/E' ratio). Although these abnormalities persisted throughout the study period in DbC, diastolic function improved with EMPA treatment. In DbC, myocardial fibrosis was accompanied by increased expression of profibrotic/prohypertrophic proteins, serum/glucocorticoid regulated kinase 1 (SGK1) and the epithelial sodium channel (ENaC), and the development of these abnormalities were reduced with EMPA. DbC exhibited eccentric LV hypertrophy that was slightly improved by EMPA, indicated by a reduction in cardiomyocyte cross sectional area. In summary, EMPA improved glycemic indices along with diastolic relaxation, as well as SGK1/ENaC profibrosis signaling and associated interstitial fibrosis, all of which occurred in the absence of any changes in BP.

Indexed as

Disease Models, AnimalSodium-Glucose Transporter 2 InhibitorsAnimalsBenzhydryl CompoundsBlood PressureDiabetes Mellitus, Type 2DiastoleFemaleGlucosidesGlycemic IndexMiceMice, Inbred C57BLMice, TransgenicSodium-Glucose Transporter 2Ventricular Function, LeftBenzhydryl CompoundsempagliflozinGlucosidesSodium-Glucose Transporter 2Sodium-Glucose Transporter 2 InhibitorsDiastolic functionEmpagliflozinSGLT2 inhibitor

Identifiers

PMID28086951
PMCPMC5237274
OpenAlexW2572657306

What OpenQuestion holds

Textmetadata
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.