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

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...

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Autores principales: Vargas-Delgado, Ariana P., Arteaga Herrera, Estefania, Tumbaco Mite, Cesar, Delgado Cedeno, Patricia, Van Loon, Maria Cristina, Badimon, Juan J.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9960541/
https://www.ncbi.nlm.nih.gov/pubmed/36835554
http://dx.doi.org/10.3390/ijms24044144
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author Vargas-Delgado, Ariana P.
Arteaga Herrera, Estefania
Tumbaco Mite, Cesar
Delgado Cedeno, Patricia
Van Loon, Maria Cristina
Badimon, Juan J.
author_facet Vargas-Delgado, Ariana P.
Arteaga Herrera, Estefania
Tumbaco Mite, Cesar
Delgado Cedeno, Patricia
Van Loon, Maria Cristina
Badimon, Juan J.
author_sort Vargas-Delgado, Ariana P.
collection PubMed
description 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.
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spelling pubmed-99605412023-02-26 Renal and Cardiovascular Metabolic Impact Caused by Ketogenesis of the SGLT2 Inhibitors Vargas-Delgado, Ariana P. Arteaga Herrera, Estefania Tumbaco Mite, Cesar Delgado Cedeno, Patricia Van Loon, Maria Cristina Badimon, Juan J. Int J Mol Sci Review 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. MDPI 2023-02-18 /pmc/articles/PMC9960541/ /pubmed/36835554 http://dx.doi.org/10.3390/ijms24044144 Text en © 2023 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).
spellingShingle Review
Vargas-Delgado, Ariana P.
Arteaga Herrera, Estefania
Tumbaco Mite, Cesar
Delgado Cedeno, Patricia
Van Loon, Maria Cristina
Badimon, Juan J.
Renal and Cardiovascular Metabolic Impact Caused by Ketogenesis of the SGLT2 Inhibitors
title Renal and Cardiovascular Metabolic Impact Caused by Ketogenesis of the SGLT2 Inhibitors
title_full Renal and Cardiovascular Metabolic Impact Caused by Ketogenesis of the SGLT2 Inhibitors
title_fullStr Renal and Cardiovascular Metabolic Impact Caused by Ketogenesis of the SGLT2 Inhibitors
title_full_unstemmed Renal and Cardiovascular Metabolic Impact Caused by Ketogenesis of the SGLT2 Inhibitors
title_short Renal and Cardiovascular Metabolic Impact Caused by Ketogenesis of the SGLT2 Inhibitors
title_sort renal and cardiovascular metabolic impact caused by ketogenesis of the sglt2 inhibitors
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9960541/
https://www.ncbi.nlm.nih.gov/pubmed/36835554
http://dx.doi.org/10.3390/ijms24044144
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