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This Article Full Text Full Text (PDF) All Versions of this Article: 584/1/235    most recent jphysiol.2007.136481v1 Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Fujiwara, Y. Articles by Tanoue, A. Search for Related Content PubMed PubMed Citation Articles by Fujiwara, Y. Articles by Tanoue, A. Related Collections Renal and Endocrine

¹ Department of Pharmacology, National Research Institute for Child Health and Development, Tokyo, Japan
² Department of Genomic Drug Discovery Science, Graduate School of Pharmaceutical Sciences, Kyoto University Faculty of Pharmaceutical Sciences, Kyoto University, Kyoto, Japan

We have reported that [Arg⁸]-vasopressin-stimulated insulin release is blunted in islet cells isolated from V1b receptor-deficient (V1bR^–/–) mice. In this study, we used V1bR^–/– mice to examine the physiological role of the V1b receptor in regulating blood glucose levels in vivo, and we found that the fasting plasma glucose, insulin and glucagon levels were lower in V1bR^–/– mice than in wild-type (V1bR^+/+) mice. Next, we evaluated glucose tolerance by performing an intraperitoneal glucose tolerance test (GTT). The plasma glucose and insulin levels during the GTT were lower in V1bR^–/– mice than in V1bR^+/+ mice. An insulin tolerance test (ITT) revealed that, after insulin administration, plasma glucose levels were lower in V1bR^–/– mice than in V1bR^+/+ mice. In addition, a hyperinsulinaemic–euglycaemic clamp study showed that the glucose infusion rate was increased in V1bR^–/– mice, indicating that insulin sensitivity was enhanced at the in vivo level in V1bR^–/– mice. Furthermore, we found that the V1b receptor was expressed in white adipose tissue and that insulin-stimulated phosphorylation of Akt as an important signaling molecule was increased in adipocytes isolated from V1bR^–/– mice. Thus, the blockade of the V1b receptor could result, at least in part, in enhanced insulin sensitivity by altering insulin signalling in adipocytes.

(Received 14 May 2007; accepted after revision 1 August 2007; first published online 2 August 2007)
Corresponding author A. Tanoue: Department of Pharmacology, National Research Institute for Child Health and Development, 2-10-1 Okura, Setagaya-ku, Tokyo 157 8535, Japan. Email: atanoue{at}nch.go.jp