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  • Title: Enhanced glucose tolerance in the Brattleboro rat.
    Author: Nakamura K, Yamashita T, Fujiki H, Aoyagi T, Yamauchi J, Mori T, Tanoue A.
    Journal: Biochem Biophys Res Commun; 2011 Feb 04; 405(1):64-7. PubMed ID: 21215256.
    Abstract:
    [Arg(8)]-vasopressin (AVP) plays a crucial role in regulating body fluid retention, which is mediated through the vasopressin V(2) receptor in the kidney. In addition, AVP is involved in the regulation of glucose homeostasis via vasopressin V(1A) and vasopressin V(1B) receptors. Our previous studies demonstrated that vasopressin V(1A) receptor-deficient (V(1A)R-/-) and V(1B) receptor-deficient (V(1B)R-/-) mice exhibited hyperglycemia and hypoglycemia with hypoinsulinemia, respectively. 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 addition, vasopressin V(1A) and vasopressin V(1B) receptor double-deficient (V(1AB)R-/-) mice exhibited impaired glucose tolerance, suggesting that the effects of vasopressin V(1B) receptor deficiency do not influence the development of hyperglycemia promoted by vasopressin V(1A) receptor deficiency, and that the blockage of both receptors could lead to impaired glucose tolerance. However, the contributions of the entire AVP/vasopressin receptors system to the regulation of blood glucose have not yet been clarified. In this study, to further understand the role of AVP/vasopressin receptors signaling in blood glucose regulation, we assessed the glucose tolerance of AVP-deficient homozygous Brattleboro (di/di) rats using an oral glucose tolerance test (GTT). Plasma glucose and insulin levels were consistently lower in homozygous di/di rats than in heterozygous di/+ rats during the GTT, suggesting that the blockage of all AVP/vasopressin receptors resulting from the AVP deficiency could lead to enhanced glucose tolerance.
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