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 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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Journal of Diabetes and its Complications, Elsevier, 2017, 31 (6), pp.929-932. 〈10.1016/j.jdiacomp.2017.04.005〉
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Ray El Boustany, Christopher Taveau, Catherine Chollet, Gilberto Velho, Lise Bankir, et al.. Antagonism of vasopressin V2 receptor improves albuminuria at the early stage of diabetic nephropathy in a mouse model of type 2 diabetes. Journal of Diabetes and its Complications, Elsevier, 2017, 31 (6), pp.929-932. 〈10.1016/j.jdiacomp.2017.04.005〉. 〈hal-01548065〉

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