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Antagonism of vasopressin V2 receptor improves albuminuria at the early stage of diabetic nephropathy in a mouse model of type 2 diabetes

Abstract Aims Vasopressin is increased in diabetes and was shown to contribute to development of diabetic nephropathy through V2 receptor (V2R) activation in an experimental model of type 1 diabetes. The role of V2R in type 2 diabetes remains undocumented. This study addresses the issue in a mouse m... Full description

Journal Title: Journal of diabetes and its complications 2017, Vol.31 (6), p.929-932
Main Author: El Boustany, Ray
Other Authors: Taveau, Christopher , Chollet, Catherine , Velho, Gilberto , Bankir, Lise , Alhenc-Gelas, François , Roussel, Ronan , Bouby, Nadine
Format: Electronic Article Electronic Article
Language: English
Subjects:
Quelle: Alma/SFX Local Collection
Publisher: United States: Elsevier Inc
ID: ISSN: 1056-8727
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title: Antagonism of vasopressin V2 receptor improves albuminuria at the early stage of diabetic nephropathy in a mouse model of type 2 diabetes
format: Article
creator:
  • El Boustany, Ray
  • Taveau, Christopher
  • Chollet, Catherine
  • Velho, Gilberto
  • Bankir, Lise
  • Alhenc-Gelas, François
  • Roussel, Ronan
  • Bouby, Nadine
subjects:
  • Albuminuria - pathology
  • Albuminuria - physiopathology
  • Albuminuria - prevention & control
  • Analysis
  • Animal experimentation
  • Animals
  • Antagonist
  • Antidiuretic Hormone Receptor Antagonists - therapeutic use
  • Blood pressure
  • Diabetes
  • Diabetes Mellitus, Experimental - complications
  • Diabetes Mellitus, Experimental - drug therapy
  • Diabetes Mellitus, Type 2 - complications
  • Diabetes Mellitus, Type 2 - drug therapy
  • Diabetic Nephropathies - drug therapy
  • Diabetic Nephropathies - pathology
  • Diabetic Nephropathies - physiopathology
  • Diabetic nephropathy
  • Endocrinology
  • Endocrinology & Metabolism
  • Endocrinology and metabolism
  • Food
  • Glomerular Filtration Rate - drug effects
  • Glucose
  • Human health
  • Human health and pathology
  • Hydration
  • Kidney diseases
  • Kidney Glomerulus - drug effects
  • Kidney Glomerulus - physiopathology
  • Life Sciences
  • Male
  • metabolism
  • Mice
  • Mice, Inbred C57BL
  • Morpholines - therapeutic use
  • Mortality
  • Nephrology
  • pathology
  • Receptors, Vasopressin - metabolism
  • Rodents
  • Spiro Compounds - therapeutic use
  • Type 2 diabetes
  • Urine
  • Urology
  • Urology and Nephrology
  • V2 receptor
  • Variance analysis
  • Vasopressin
ispartof: Journal of diabetes and its complications, 2017, Vol.31 (6), p.929-932
description: Abstract Aims Vasopressin is increased in diabetes and was shown to contribute to development of diabetic nephropathy through V2 receptor (V2R) activation in an experimental model of type 1 diabetes. The role of V2R in type 2 diabetes remains undocumented. This study addresses the issue in a mouse model of type 2 diabetes. Methods Male obese diabetic db/db mice were treated for 12 weeks with a selective V2R antagonist ( SR121463 ) and compared to non-treated db/db and non-diabetic db/m mice. All animals were previously uninephrectomized. Results The V2R antagonist did not alter glycemia or glycosuria in db/db mice. It induced a two-fold increase in urine output and a 52% decrease in urine osmolality compared to non-treated db/db mice. After four weeks of treatment urinary albumin to creatinine ratio was 50% lower in treated mice compared to non-treated mice, and remained significantly lower until end of experiment. Glomerular filtration rate increased significantly over time in non-treated db/db mice but remained stable in treated mice. Conclusions This study shows that vasopressin contributes to albuminuria and glomerular hyperfiltration via V2R in a mouse model of type 2 diabetes. It documents causality behind the association of vasopressin with renal disease observed in diabetic patients.
language: eng
source: Alma/SFX Local Collection
identifier: ISSN: 1056-8727
fulltext: fulltext
issn:
  • 1056-8727
  • 1873-460X
url: Link


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titleAntagonism of vasopressin V2 receptor improves albuminuria at the early stage of diabetic nephropathy in a mouse model of type 2 diabetes
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creatorEl Boustany, Ray ; Taveau, Christopher ; Chollet, Catherine ; Velho, Gilberto ; Bankir, Lise ; Alhenc-Gelas, François ; Roussel, Ronan ; Bouby, Nadine
creatorcontribEl Boustany, Ray ; Taveau, Christopher ; Chollet, Catherine ; Velho, Gilberto ; Bankir, Lise ; Alhenc-Gelas, François ; Roussel, Ronan ; Bouby, Nadine
descriptionAbstract Aims Vasopressin is increased in diabetes and was shown to contribute to development of diabetic nephropathy through V2 receptor (V2R) activation in an experimental model of type 1 diabetes. The role of V2R in type 2 diabetes remains undocumented. This study addresses the issue in a mouse model of type 2 diabetes. Methods Male obese diabetic db/db mice were treated for 12 weeks with a selective V2R antagonist ( SR121463 ) and compared to non-treated db/db and non-diabetic db/m mice. All animals were previously uninephrectomized. Results The V2R antagonist did not alter glycemia or glycosuria in db/db mice. It induced a two-fold increase in urine output and a 52% decrease in urine osmolality compared to non-treated db/db mice. After four weeks of treatment urinary albumin to creatinine ratio was 50% lower in treated mice compared to non-treated mice, and remained significantly lower until end of experiment. Glomerular filtration rate increased significantly over time in non-treated db/db mice but remained stable in treated mice. Conclusions This study shows that vasopressin contributes to albuminuria and glomerular hyperfiltration via V2R in a mouse model of type 2 diabetes. It documents causality behind the association of vasopressin with renal disease observed in diabetic patients.
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0ISSN: 1056-8727
1EISSN: 1873-460X
2DOI: 10.1016/j.jdiacomp.2017.04.005
3PMID: 28412033
languageeng
publisherUnited States: Elsevier Inc
subjectAlbuminuria - pathology ; Albuminuria - physiopathology ; Albuminuria - prevention & control ; Analysis ; Animal experimentation ; Animals ; Antagonist ; Antidiuretic Hormone Receptor Antagonists - therapeutic use ; Blood pressure ; Diabetes ; Diabetes Mellitus, Experimental - complications ; Diabetes Mellitus, Experimental - drug therapy ; Diabetes Mellitus, Type 2 - complications ; Diabetes Mellitus, Type 2 - drug therapy ; Diabetic Nephropathies - drug therapy ; Diabetic Nephropathies - pathology ; Diabetic Nephropathies - physiopathology ; Diabetic nephropathy ; Endocrinology ; Endocrinology & Metabolism ; Endocrinology and metabolism ; Food ; Glomerular Filtration Rate - drug effects ; Glucose ; Human health ; Human health and pathology ; Hydration ; Kidney diseases ; Kidney Glomerulus - drug effects ; Kidney Glomerulus - physiopathology ; Life Sciences ; Male ; metabolism ; Mice ; Mice, Inbred C57BL ; Morpholines - therapeutic use ; Mortality ; Nephrology ; pathology ; Receptors, Vasopressin - metabolism ; Rodents ; Spiro Compounds - therapeutic use ; Type 2 diabetes ; Urine ; Urology ; Urology and Nephrology ; V2 receptor ; Variance analysis ; Vasopressin
ispartofJournal of diabetes and its complications, 2017, Vol.31 (6), p.929-932
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0Elsevier Inc.
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3COPYRIGHT 2017 Elsevier B.V.
4Copyright Elsevier Limited Jun 1, 2017
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0El Boustany, Ray
1Taveau, Christopher
2Chollet, Catherine
3Velho, Gilberto
4Bankir, Lise
5Alhenc-Gelas, François
6Roussel, Ronan
7Bouby, Nadine
title
0Antagonism of vasopressin V2 receptor improves albuminuria at the early stage of diabetic nephropathy in a mouse model of type 2 diabetes
1Journal of diabetes and its complications
addtitleJ Diabetes Complications
descriptionAbstract Aims Vasopressin is increased in diabetes and was shown to contribute to development of diabetic nephropathy through V2 receptor (V2R) activation in an experimental model of type 1 diabetes. The role of V2R in type 2 diabetes remains undocumented. This study addresses the issue in a mouse model of type 2 diabetes. Methods Male obese diabetic db/db mice were treated for 12 weeks with a selective V2R antagonist ( SR121463 ) and compared to non-treated db/db and non-diabetic db/m mice. All animals were previously uninephrectomized. Results The V2R antagonist did not alter glycemia or glycosuria in db/db mice. It induced a two-fold increase in urine output and a 52% decrease in urine osmolality compared to non-treated db/db mice. After four weeks of treatment urinary albumin to creatinine ratio was 50% lower in treated mice compared to non-treated mice, and remained significantly lower until end of experiment. Glomerular filtration rate increased significantly over time in non-treated db/db mice but remained stable in treated mice. Conclusions This study shows that vasopressin contributes to albuminuria and glomerular hyperfiltration via V2R in a mouse model of type 2 diabetes. It documents causality behind the association of vasopressin with renal disease observed in diabetic patients.
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0Albuminuria - pathology
1Albuminuria - physiopathology
2Albuminuria - prevention & control
3Analysis
4Animal experimentation
5Animals
6Antagonist
7Antidiuretic Hormone Receptor Antagonists - therapeutic use
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12Diabetes Mellitus, Type 2 - complications
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14Diabetic Nephropathies - drug therapy
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17Diabetic nephropathy
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19Endocrinology & Metabolism
20Endocrinology and metabolism
21Food
22Glomerular Filtration Rate - drug effects
23Glucose
24Human health
25Human health and pathology
26Hydration
27Kidney diseases
28Kidney Glomerulus - drug effects
29Kidney Glomerulus - physiopathology
30Life Sciences
31Male
32metabolism
33Mice
34Mice, Inbred C57BL
35Morpholines - therapeutic use
36Mortality
37Nephrology
38pathology
39Receptors, Vasopressin - metabolism
40Rodents
41Spiro Compounds - therapeutic use
42Type 2 diabetes
43Urine
44Urology
45Urology and Nephrology
46V2 receptor
47Variance analysis
48Vasopressin
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titleAntagonism of vasopressin V2 receptor improves albuminuria at the early stage of diabetic nephropathy in a mouse model of type 2 diabetes
authorEl Boustany, Ray ; Taveau, Christopher ; Chollet, Catherine ; Velho, Gilberto ; Bankir, Lise ; Alhenc-Gelas, François ; Roussel, Ronan ; Bouby, Nadine
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1Albuminuria - physiopathology
2Albuminuria - prevention & control
3Analysis
4Animal experimentation
5Animals
6Antagonist
7Antidiuretic Hormone Receptor Antagonists - therapeutic use
8Blood pressure
9Diabetes
10Diabetes Mellitus, Experimental - complications
11Diabetes Mellitus, Experimental - drug therapy
12Diabetes Mellitus, Type 2 - complications
13Diabetes Mellitus, Type 2 - drug therapy
14Diabetic Nephropathies - drug therapy
15Diabetic Nephropathies - pathology
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30Life Sciences
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35Morpholines - therapeutic use
36Mortality
37Nephrology
38pathology
39Receptors, Vasopressin - metabolism
40Rodents
41Spiro Compounds - therapeutic use
42Type 2 diabetes
43Urine
44Urology
45Urology and Nephrology
46V2 receptor
47Variance analysis
48Vasopressin
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1Taveau, Christopher
2Chollet, Catherine
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jtitleJournal of diabetes and its complications
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abstractAbstract Aims Vasopressin is increased in diabetes and was shown to contribute to development of diabetic nephropathy through V2 receptor (V2R) activation in an experimental model of type 1 diabetes. The role of V2R in type 2 diabetes remains undocumented. This study addresses the issue in a mouse model of type 2 diabetes. Methods Male obese diabetic db/db mice were treated for 12 weeks with a selective V2R antagonist ( SR121463 ) and compared to non-treated db/db and non-diabetic db/m mice. All animals were previously uninephrectomized. Results The V2R antagonist did not alter glycemia or glycosuria in db/db mice. It induced a two-fold increase in urine output and a 52% decrease in urine osmolality compared to non-treated db/db mice. After four weeks of treatment urinary albumin to creatinine ratio was 50% lower in treated mice compared to non-treated mice, and remained significantly lower until end of experiment. Glomerular filtration rate increased significantly over time in non-treated db/db mice but remained stable in treated mice. Conclusions This study shows that vasopressin contributes to albuminuria and glomerular hyperfiltration via V2R in a mouse model of type 2 diabetes. It documents causality behind the association of vasopressin with renal disease observed in diabetic patients.
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