Both V1A and V1B vasopressin receptors deficiency result in impaired glucose tolerance
Abstract
[Arg(8)]-vasopressin (AVP) is involved in the regulation of glucose homeostasis via vasopressin V(1A) and vasopressin V(1B) receptor. Our previous studies have demonstrated that vasopressin V(1A) receptor deficient (V(1A)R(-/-)) mice exhibited hyperglycemia, vasopressin V(1B) receptor deficient (V(1B)R(-/-)) mice, in contrast, exhibited hypoglycemia with hypoinsulinemia. These findings indicate that vasopressin V(1A) receptor deficiency results in decreased insulin sensitivity, whereas vasopressin V(1B) receptor deficiency results in increased insulin sensitivity. In our previous and present studies, we used the glucose tolerance test to investigate glucose tolerance in mutant mice, lacking either the vasopressin V(1A) receptor, the vasopressin V(1B) receptor, or both receptors, that were kept on a high-fat diet. Glucose and insulin levels were lower in V(1B)R(-/-) mice than in wild type (WT) mice when both groups were fed the high-fat diet, which indicates that the insulin sensitivity of the V(1B)R(-/-) mice was enhanced. V(1A)R(-/-) mice on the high-fat diet, on the other hand, exhibited overt obesity, along with an impaired glucose tolerance, while WT mice on the high-fat diet did not. Next, in order to assess the effect of vasopressin V(1B) receptor deficiency on the development of glucose intolerance caused by vasopressin V(1A) receptor deficiency, we generated mice that were deficient for both vasopressin V(1A) receptor and vasopressin V(1B) receptor (V(1AB)R(-/-)), fed them a high-fat diet, and examined their glucose tolerances using the glucose tolerance test. Glucose tolerance was impaired in V(1AB)R(-/-) mice, suggesting that the effects of vasopressin V(1B) receptor deficiency could not influence the development of hyperglycemia promoted by vasopressin V(1A) receptor deficiency, and that blockade of both receptors could lead to impaired glucose tolerance.
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Mice with deleted V1a and/or V1b receptors exhibit metabolic disorders.
“The finding that mice with deleted V1aR and/or V1bR exhibit metabolic disorders [12][13][14][15] has prompted several epidemiological investigations in humans.”
From Vasopressin and hydration play a major role in the development of glucose intolerance and hepatic steatosis in obese rats (2015) · cites this paper as [14]
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- Authors
- Nakamura, K., Aoyagi, T., Hiroyama, M., Kusakawa, S., Mizutani, R., Sanbe, A., Yamauchi, J., Kamohara, M., Momose, K., & Tanoue, A.
- Affiliations
- National Research Institute for Child Health and Development (JP)
- Astellas Pharma (Japan) (JP)
- Corresponding author
- Tanoue, Akito
- Venue
- European Journal of Pharmacology
- Publisher
- Elsevier BV
- Published
- 2009-06
- Volume
- 613
- Issue
- 1-3
- Pages
- 182-188
- ISSN
- 0014-2999 (ISSN-L)
- OpenAlex
- W2007102871
- Cited by
- 41
- References
- 29
- Citations by year
- 2026: 2 · 2025: 1 · 2024: 4 · 2023: 2 · 2021: 4 · 2020: 1 · 2019: 2 · 2018: 3 · 2017: 6 · 2016: 2 · 2015: 5 · 2013: 3 · 2012: 2
- FWCI
- 2.02
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- European Journal of Pharmacology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Ministry of Education, Culture, Sports, Science and Technology
- Topics
- Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
- Social Sciences › Psychology › Social Psychology › Neuroendocrine regulation and behavior
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
- Keywords
- vasopressin V1a receptor, vasopressin V1b receptor, vasopressin, glucose tolerance, glucose homeostasis, insulin sensitivity, hyperglycemia, hypoglycemia, high-fat diet, obesity, receptor knockout mice
- MeSH terms
- Animals, Blood Glucose, Body Weight, Energy Intake, Dietary Fats, Homeostasis, Insulin, Male, Phosphorylation, Receptors, Vasopressin, Glucose Intolerance, Proto-Oncogene Proteins c-akt, Mice, Adipocytes, White
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