EMPAGLIFLOZIN INDUCES A MYOCARDIAL METABOLIC SHIFT FROM GLUCOSE CONSUMPTION TO KETONE METABOLISM THAT MITIGATES ADVERSE CARDIAC REMODELING AND IMPROVES MYOCARDIAL CONTRACTILITY

Carlos G. Santos-Gallego,Juan Antonio Requena Ibanez,Rodolfo San Antonio,Kiyotake Ishikawa,Shin Watanabe,Maria Belen Picatoste Botija,Angel Sanz Salvo,Roger J. Hajjar,Valentin Fuster,Juan J. Badimon

EMPAGLIFLOZIN INDUCES A MYOCARDIAL METABOLIC SHIFT FROM GLUCOSE CONSUMPTION TO KETONE METABOLISM THAT MITIGATES ADVERSE CARDIAC REMODELING AND IMPROVES MYOCARDIAL CONTRACTILITY

2018

Carlos G. Santos-Gallego
Juan Antonio Requena Ibanez
Rodolfo San Antonio
Kiyotake Ishikawa
Shin Watanabe
Maria Belen Picatoste Botija
Angel Sanz Salvo
Roger J. Hajjar
Valentin Fuster
Juan J. Badimon

Mechanisms behind heart failure reduction with SGLT2 inhibitor empagliflozin (EMPA) in clinical trials remain unclear. Given that EMPA causes mild, persistent hyperketonemia, we hypothesized that cardiac benefits of EMPA are due to a shift in myocardial fuel metabolism away from glucose oxidation (

Keywords:

SGLT2 Inhibitor
Ketone bodies
Metabolism
EMPA
Contractility
Diabetes mellitus
Internal medicine
Cardiology
Heart failure
Empagliflozin
Medicine

Correction
Source
Cite
Save
Machine Reading By IdeaReader

References

Citations