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Review

Renal and Cardiovascular Metabolic Impact Caused by Ketogenesis of the SGLT2 Inhibitors

by
Ariana P. Vargas-Delgado
1,2,*,
Estefania Arteaga Herrera
2,
Cesar Tumbaco Mite
2,
Patricia Delgado Cedeno
2,
Maria Cristina Van Loon
2 and
Juan J. Badimon
1
1
AtheroThrombosis Research Unit, Mount Sinai Heart, Icahn School of Medicine at Mount Sinai, One Gustave L. Levy Place, New York, NY 10029, USA
2
Instituto Ecuatoriano del Corazón (IECOR), Guayaquil 090513, Ecuador
*
Author to whom correspondence should be addressed.
Int. J. Mol. Sci. 2023, 24(4), 4144; https://doi.org/10.3390/ijms24044144
Submission received: 2 January 2023 / Revised: 13 February 2023 / Accepted: 15 February 2023 / Published: 18 February 2023
(This article belongs to the Special Issue Molecular Mechanisms of Cardiac Development and Disease)

Abstract

Sodium–glucose cotransporter type 2 inhibitors (SGLT2i) are glycosuric drugs that were originally developed for the treatment of type 2 diabetes mellitus (T2DM). There is a hypothesis that SGLT2i are drugs that are capable of increasing ketone bodies and free fatty acids. The idea is that they could serve as the necessary fuel, instead of glucose, for the purposes of cardiac muscle requirements and could explain antihypertensive effects, which are independent of renal function. The adult heart, under normal conditions, consumes around 60% to 90% of the cardiac energy that is derived from the oxidation of free fatty acids. In addition, a small proportion also comes from other available substrates. In order to meet energy demands with respect to achieving adequate cardiac function, the heart is known to possess metabolic flexibility. This allows it to switch between different available substrates in order to obtain the energy molecule adenosine triphosphate (ATP), thereby rendering it highly adaptive. It must be noted that oxidative phosphorylation in aerobic organisms is the main source of ATP, which is a result of reduced cofactors. These cofactors include nicotine adenine dinucleotide (NADH) and flavin adenine dinucleotide (FADH2), which are the result of electron transfer and are used as the enzymatic cofactors that are involved in the respiratory chain. When there is an excessive increase in energy nutrients—such as glucose and fatty acids—which occur in the absence of a parallel increase in demand, a state of nutrient surplus (which is better known as an excess in supply) is created. The use of SGLT2i at the renal level has also been shown to generate beneficial metabolic alterations, which are obtained by reducing the glucotoxicity that is induced by glycosuria. Together with the reduction in perivisceral fat in various organs, such alterations also lead to the use of free fatty acids in the initial stages of the affected heart. Subsequently, this results in an increase in production with respect to ketoacids, which are a more available energy fuel at the cellular level. In addition, even though their mechanism is not fully understood, their vast benefits render them of incredible importance for the purposes of further research.
Keywords: sodium–glucose cotransporter type 2 inhibitors; type 2 diabetes mellitus; heart failure; ketone bodies; free fatty acids; chronic kidney disease; arterial stiffness sodium–glucose cotransporter type 2 inhibitors; type 2 diabetes mellitus; heart failure; ketone bodies; free fatty acids; chronic kidney disease; arterial stiffness

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MDPI and ACS Style

Vargas-Delgado, A.P.; Arteaga Herrera, E.; Tumbaco Mite, C.; Delgado Cedeno, P.; Van Loon, M.C.; Badimon, J.J. Renal and Cardiovascular Metabolic Impact Caused by Ketogenesis of the SGLT2 Inhibitors. Int. J. Mol. Sci. 2023, 24, 4144. https://doi.org/10.3390/ijms24044144

AMA Style

Vargas-Delgado AP, Arteaga Herrera E, Tumbaco Mite C, Delgado Cedeno P, Van Loon MC, Badimon JJ. Renal and Cardiovascular Metabolic Impact Caused by Ketogenesis of the SGLT2 Inhibitors. International Journal of Molecular Sciences. 2023; 24(4):4144. https://doi.org/10.3390/ijms24044144

Chicago/Turabian Style

Vargas-Delgado, Ariana P., Estefania Arteaga Herrera, Cesar Tumbaco Mite, Patricia Delgado Cedeno, Maria Cristina Van Loon, and Juan J. Badimon. 2023. "Renal and Cardiovascular Metabolic Impact Caused by Ketogenesis of the SGLT2 Inhibitors" International Journal of Molecular Sciences 24, no. 4: 4144. https://doi.org/10.3390/ijms24044144

APA Style

Vargas-Delgado, A. P., Arteaga Herrera, E., Tumbaco Mite, C., Delgado Cedeno, P., Van Loon, M. C., & Badimon, J. J. (2023). Renal and Cardiovascular Metabolic Impact Caused by Ketogenesis of the SGLT2 Inhibitors. International Journal of Molecular Sciences, 24(4), 4144. https://doi.org/10.3390/ijms24044144

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