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Insulin hypersensitivity in mice lacking the V1b vasopressin receptor
Author(s) -
Fujiwara Yoko,
Hiroyama Masami,
Sanbe Atsushi,
Aoyagi Toshinori,
Birumachi Junichi,
Yamauchi Junji,
Tsujimoto Gozoh,
Tanoue Akito
Publication year - 2007
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.2007.136481
Subject(s) - insulin receptor , medicine , insulin , endocrinology , glucagon like peptide 1 receptor , adipose tissue , receptor , biology , insulin resistance , agonist
We have reported that [Arg 8 ]‐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.