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Submitted on September 25, 2006
Accepted on February 2, 2007
Department of Pharmacology, National Research Institute for Child Health and Development, 2-10-1, Okura, Setagaya-ku, Tokyo 157-8535, Japan
* To whom correspondence should be addressed. E-mail: atanoue{at}nch.go.jp.
Arginine-vasopressin (AVP) is known to be involved in maintaining glucose homeostasis, and AVP-resistance is observed in poorly controlled NIDDM subjects, resulting in a lowered plasma volume. Recently, we reported that V1a vasopressin receptor-deficient (V1aR-/-) mice exhibited a decreased circulating blood volume and hypermetabolism of fat accompanied with impaired insulin-signaling. Here, we further investigated the roles of the AVP/V1a receptor in regulating glucose homeostasis and plasma volume using V1aR-/- mice. The plasma glucose levels at the baseline or during a GTT were higher in V1aR-/- than in WT mice. Moreover, a hyperinsulinemic-euglycemic clamp revealed that the glucose infusion rate was significantly lower in V1aR-/- mice than in WT mice and that hepatic glucose production was higher in V1aR-/- mice than in WT mice. In contrast to the increased hepatic glucose production, the liver glycogen content was decreased in the mutant mice. These results indicated that the mutant mice had impaired glucose tolerance. Furthermore, feeding V1aR-/- mice a high-fat-diet accompanied with increased calorie intake resulted in significantly overt obesity in comparison with WT mice. In addition, we found that the circulating plasma volume and aldosterone level were decreased in V1aR-/- mice, although the plasma AVP level was increased. These results suggested that the effect of AVP on water recruitment was disturbed in V1aR-/- mice. Thus, we demonstrated that one of the AVP-resistance conditions resulting from deficiency of the V1a receptor leads to decreased plasma volume as well as impaired glucose homeostasis, which can progress to obesity under conditions of increased calorie intake.
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