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Cited by 110Chronic Kidney Disease and DiabetesElectrolyte and hormonal disordersIon Transport and Channel Regulation

Vasopressin and diabetes mellitus

Bankir, Lise, Bardoux, Pascale, Ahloulay, Mina·2001·Nephron
DOI 10.1159/000045879
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Abstract

In diabetes mellitus (DM), the urine flow rate is increased, and the fluid turnover in the body is accelerated because of the glucose-induced osmotic diuresis. On the other hand, plasma vasopressin (VP) is elevated in both type 1 and type 2 DM. This elevation seems to be due to a resetting of the osmostat. A high VP level is beneficial in the short term because it limits to some extent the amount of water required for the excretion of a markedly enhanced load of osmoles (mainly glucose). However, in the long run, it may have adverse effects by favoring the developement of diabetic nephropathy. VP has been shown in normal rats to induce kidney hypertrophy, glomerular hyperfiltration, and an increase in urinary albumin excretion (features also occurring in association in the period preceding diabetic nephropathy). Moreover, VP has been shown to participate in the progression of renal failure in rats with five-sixths reduction in renal mass. In recent studies, we have shown (1) that creatinine clearance, albuminuria and renal mass increased much less during experimental DM in Brattleboro rats unable to secrete VP than in their VP-replete Long-Evans controls, and (2) that albuminuria was prevented during experimental DM in Wistar rats when a VP nonpeptidic, highly selective V2 receptor antagonist was administered chronically for 9 weeks. Taken together, these results strongly suggest that VP plays a crucial role in the onset and aggravation of the renal complications of DM. The mechanisms by which VP exerts these adverse V2-dependent effects are not yet elucidated. They are most likely indirect and may involve several intermediate steps comprising VP-induced changes in the composition of the tubular fluid in the loop of Henle (due to solute recycling in the renal medulla associated with improved concentrating activity of the kidney), inhibition of the tubuloglomerular feedback control of glomerular function, and alterations in glomerular hemodynamics by the intrarenal renin-angiotensin system.

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Crossref · 10.1159/000045879

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66 of 66 references verified0 citation errors · 0 not checkable

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  • Vasopressin receptors are expressed in hepatocytes and pancreatic islets.

    “A causal link between vasopressin and glucose homeostasis is plausible because vasopressin induces gluconeogenesis in the rat liver and transiently increases glycemia in healthy humans and because vasopressin receptors are expressed in hepatocytes and pancreatic islets (2–9).”

    From Low Water Intake and Risk for New-Onset Hyperglycemia (2011) · cites this paper as [3]

  • A causal link between vasopressin and glucose homeostasis is plausible.

    “A causal link between vasopressin and glucose homeostasis is plausible because vasopressin induces gluconeogenesis in the rat liver and transiently increases glycemia in healthy humans and because vasopressin receptors are expressed in hepatocytes and pancreatic islets (2–9).”

    From Low Water Intake and Risk for New-Onset Hyperglycemia (2011) · cites this paper as [3]

  • Vasopressin transiently increases glycemia in healthy humans.

    “A causal link between vasopressin and glucose homeostasis is plausible because vasopressin induces gluconeogenesis in the rat liver and transiently increases glycemia in healthy humans and because vasopressin receptors are expressed in hepatocytes and pancreatic islets (2–9).”

    From Low Water Intake and Risk for New-Onset Hyperglycemia (2011) · cites this paper as [3]

  • Vasopressin induces gluconeogenesis in the rat liver.

    “A causal link between vasopressin and glucose homeostasis is plausible because vasopressin induces gluconeogenesis in the rat liver and transiently increases glycemia in healthy humans and because vasopressin receptors are expressed in hepatocytes and pancreatic islets (2–9).”

    From Low Water Intake and Risk for New-Onset Hyperglycemia (2011) · cites this paper as [3]

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Authors
Bankir, L., Bardoux, P., & Ahloulay, M.
Affiliations
Inserm (FR)
ORCID
Bankir, Lise
Venue
Nephron
Publisher
S. Karger AG
Published
2001
Volume
87
Issue
1
Pages
8-18
ISSN
  • 1660-8151 (ISSN-L)
  • 2235-3186
DOI
10.1159/000045879
OpenAlex
W2037060198
Cited by
110
References
66
Citations by year
2026: 1 · 2025: 3 · 2024: 3 · 2023: 8 · 2022: 2 · 2021: 2 · 2020: 4 · 2019: 5 · 2018: 8 · 2017: 8 · 2016: 8 · 2015: 5 · 2014: 3 · 2013: 5 · 2012: 3
FWCI
3.60
Type
journal article
Language
en
Open access
closed
Licence
Locations
  • The Nephron journals/Nephron journals (publishedVersion)
  • PubMed (publishedVersion)
Funders
Institut National de la Santé et de la Recherche Médicale
Topics
  • Health Sciences › Medicine › Nephrology › Chronic Kidney Disease and Diabetes
  • Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Electrolyte and hormonal disorders
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Ion Transport and Channel Regulation
Keywords
vasopressin, diabetes mellitus, diabetic nephropathy, osmotic diuresis, vasopressin V2 receptor antagonist, albuminuria, renal hypertrophy, glomerular hyperfiltration, tubuloglomerular feedback, intrarenal renin-angiotensin system, loop of Henle, Brattleboro rats, Long-Evans rats
MeSH terms
Diabetes Mellitus, Type 1, Diabetes Mellitus, Type 2, Humans, Vasopressins

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