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Metabolic effects of vasopressin in pathophysiology of diabetic kidney disease

The diabetic kidney disease (DKD) is the major cause of the chronic kidney disease (CKD). Enhanced plasma vasopressin (VP) levels have been associated with the pathophysiology of DKD and CKD. Stimulation of VP release in DKD is caused by glucose-dependent reset of the osmostat leading to secondary p...

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Autores principales: Lebedeva, Svetlana, Margaryan, Arus, Smolyarchuk, Elena, Nedorubov, Andrey, Materenchuk, Maria, Tonevitsky, Alexander, Mutig, Kerim
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10545091/
https://www.ncbi.nlm.nih.gov/pubmed/37790608
http://dx.doi.org/10.3389/fendo.2023.1176199
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author Lebedeva, Svetlana
Margaryan, Arus
Smolyarchuk, Elena
Nedorubov, Andrey
Materenchuk, Maria
Tonevitsky, Alexander
Mutig, Kerim
author_facet Lebedeva, Svetlana
Margaryan, Arus
Smolyarchuk, Elena
Nedorubov, Andrey
Materenchuk, Maria
Tonevitsky, Alexander
Mutig, Kerim
author_sort Lebedeva, Svetlana
collection PubMed
description The diabetic kidney disease (DKD) is the major cause of the chronic kidney disease (CKD). Enhanced plasma vasopressin (VP) levels have been associated with the pathophysiology of DKD and CKD. Stimulation of VP release in DKD is caused by glucose-dependent reset of the osmostat leading to secondary pathophysiologic effects mediated by distinct VP receptor types. VP is a stress hormone exhibiting the antidiuretic action in the kidney along with broad adaptive effects in other organs. Excessive activation of the vasopressin type 2 (V2) receptor in the kidney leads to glomerular hyperfiltration and nephron loss, whereas stimulation of vasopressin V1a or V1b receptors in the liver, pancreas, and adrenal glands promotes catabolic metabolism for energy mobilization, enhancing glucose production and aggravating DKD. Increasing availability of selective VP receptor antagonists opens new therapeutic windows separating the renal and extra-renal VP effects for the concrete applications. Improved understanding of these paradigms is mandatory for further drug design and translational implementation. The present concise review focuses on metabolic effects of VP affecting DKD pathophysiology.
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spelling pubmed-105450912023-10-03 Metabolic effects of vasopressin in pathophysiology of diabetic kidney disease Lebedeva, Svetlana Margaryan, Arus Smolyarchuk, Elena Nedorubov, Andrey Materenchuk, Maria Tonevitsky, Alexander Mutig, Kerim Front Endocrinol (Lausanne) Endocrinology The diabetic kidney disease (DKD) is the major cause of the chronic kidney disease (CKD). Enhanced plasma vasopressin (VP) levels have been associated with the pathophysiology of DKD and CKD. Stimulation of VP release in DKD is caused by glucose-dependent reset of the osmostat leading to secondary pathophysiologic effects mediated by distinct VP receptor types. VP is a stress hormone exhibiting the antidiuretic action in the kidney along with broad adaptive effects in other organs. Excessive activation of the vasopressin type 2 (V2) receptor in the kidney leads to glomerular hyperfiltration and nephron loss, whereas stimulation of vasopressin V1a or V1b receptors in the liver, pancreas, and adrenal glands promotes catabolic metabolism for energy mobilization, enhancing glucose production and aggravating DKD. Increasing availability of selective VP receptor antagonists opens new therapeutic windows separating the renal and extra-renal VP effects for the concrete applications. Improved understanding of these paradigms is mandatory for further drug design and translational implementation. The present concise review focuses on metabolic effects of VP affecting DKD pathophysiology. Frontiers Media S.A. 2023-09-18 /pmc/articles/PMC10545091/ /pubmed/37790608 http://dx.doi.org/10.3389/fendo.2023.1176199 Text en Copyright © 2023 Lebedeva, Margaryan, Smolyarchuk, Nedorubov, Materenchuk, Tonevitsky and Mutig https://creativecommons.org/licenses/by/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Endocrinology
Lebedeva, Svetlana
Margaryan, Arus
Smolyarchuk, Elena
Nedorubov, Andrey
Materenchuk, Maria
Tonevitsky, Alexander
Mutig, Kerim
Metabolic effects of vasopressin in pathophysiology of diabetic kidney disease
title Metabolic effects of vasopressin in pathophysiology of diabetic kidney disease
title_full Metabolic effects of vasopressin in pathophysiology of diabetic kidney disease
title_fullStr Metabolic effects of vasopressin in pathophysiology of diabetic kidney disease
title_full_unstemmed Metabolic effects of vasopressin in pathophysiology of diabetic kidney disease
title_short Metabolic effects of vasopressin in pathophysiology of diabetic kidney disease
title_sort metabolic effects of vasopressin in pathophysiology of diabetic kidney disease
topic Endocrinology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10545091/
https://www.ncbi.nlm.nih.gov/pubmed/37790608
http://dx.doi.org/10.3389/fendo.2023.1176199
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