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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...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Frontiers Media S.A.
2023
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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. |
format | Online Article Text |
id | pubmed-10545091 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | Frontiers Media S.A. |
record_format | MEDLINE/PubMed |
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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