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Novel Hypothesis to Explain Why SGLT2 Inhibitors Inhibit Only 30–50% of Filtered Glucose Load in Humans

Inhibitors of sodium-glucose cotransporter 2 (SGLT2) are a novel class of antidiabetes drugs, and members of this class are under various stages of clinical development for the management of type 2 diabetes mellitus (T2DM). It is widely accepted that SGLT2 is responsible for >80% of the reabsorpt...

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Detalles Bibliográficos
Autores principales: Abdul-Ghani, Muhammad A., DeFronzo, Ralph A., Norton, Luke
Formato: Online Artículo Texto
Lenguaje:English
Publicado: American Diabetes Association 2013
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3781482/
https://www.ncbi.nlm.nih.gov/pubmed/24065789
http://dx.doi.org/10.2337/db13-0604
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author Abdul-Ghani, Muhammad A.
DeFronzo, Ralph A.
Norton, Luke
author_facet Abdul-Ghani, Muhammad A.
DeFronzo, Ralph A.
Norton, Luke
author_sort Abdul-Ghani, Muhammad A.
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description Inhibitors of sodium-glucose cotransporter 2 (SGLT2) are a novel class of antidiabetes drugs, and members of this class are under various stages of clinical development for the management of type 2 diabetes mellitus (T2DM). It is widely accepted that SGLT2 is responsible for >80% of the reabsorption of the renal filtered glucose load. However, maximal doses of SGLT2 inhibitors fail to inhibit >50% of the filtered glucose load. Because the clinical efficacy of this group of drugs is entirely dependent on the amount of glucosuria produced, it is important to understand why SGLT2 inhibitors inhibit <50% of the filtered glucose load. In this Perspective, we provide a novel hypothesis that explains this apparent puzzle and discuss some of the clinical implications inherent in this hypothesis.
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spelling pubmed-37814822014-10-01 Novel Hypothesis to Explain Why SGLT2 Inhibitors Inhibit Only 30–50% of Filtered Glucose Load in Humans Abdul-Ghani, Muhammad A. DeFronzo, Ralph A. Norton, Luke Diabetes Perspectives in Diabetes Inhibitors of sodium-glucose cotransporter 2 (SGLT2) are a novel class of antidiabetes drugs, and members of this class are under various stages of clinical development for the management of type 2 diabetes mellitus (T2DM). It is widely accepted that SGLT2 is responsible for >80% of the reabsorption of the renal filtered glucose load. However, maximal doses of SGLT2 inhibitors fail to inhibit >50% of the filtered glucose load. Because the clinical efficacy of this group of drugs is entirely dependent on the amount of glucosuria produced, it is important to understand why SGLT2 inhibitors inhibit <50% of the filtered glucose load. In this Perspective, we provide a novel hypothesis that explains this apparent puzzle and discuss some of the clinical implications inherent in this hypothesis. American Diabetes Association 2013-10 2013-09-17 /pmc/articles/PMC3781482/ /pubmed/24065789 http://dx.doi.org/10.2337/db13-0604 Text en © 2013 by the American Diabetes Association. Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work is not altered. See http://creativecommons.org/licenses/by-nc-nd/3.0/ for details.
spellingShingle Perspectives in Diabetes
Abdul-Ghani, Muhammad A.
DeFronzo, Ralph A.
Norton, Luke
Novel Hypothesis to Explain Why SGLT2 Inhibitors Inhibit Only 30–50% of Filtered Glucose Load in Humans
title Novel Hypothesis to Explain Why SGLT2 Inhibitors Inhibit Only 30–50% of Filtered Glucose Load in Humans
title_full Novel Hypothesis to Explain Why SGLT2 Inhibitors Inhibit Only 30–50% of Filtered Glucose Load in Humans
title_fullStr Novel Hypothesis to Explain Why SGLT2 Inhibitors Inhibit Only 30–50% of Filtered Glucose Load in Humans
title_full_unstemmed Novel Hypothesis to Explain Why SGLT2 Inhibitors Inhibit Only 30–50% of Filtered Glucose Load in Humans
title_short Novel Hypothesis to Explain Why SGLT2 Inhibitors Inhibit Only 30–50% of Filtered Glucose Load in Humans
title_sort novel hypothesis to explain why sglt2 inhibitors inhibit only 30–50% of filtered glucose load in humans
topic Perspectives in Diabetes
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3781482/
https://www.ncbi.nlm.nih.gov/pubmed/24065789
http://dx.doi.org/10.2337/db13-0604
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