Enhanced glucose tolerance in the Brattleboro rat
Kazuaki Nakamura1, Tatsuya Yamashita, Hiroyuki Fujiki
1Department of Pharmacology, National Research Institute for Child Health and Development, Tokyo, Japan.
Biochemical and Biophysical Research Communications
|January 11, 2011
Summary
[Arg(8)]-vasopressin (AVP) deficiency in rats enhances glucose tolerance by affecting all AVP/vasopressin receptors. This suggests a crucial role for the AVP system in regulating blood glucose levels.
Area of Science:
- Endocrinology
- Metabolism
- Physiology
Background:
- [Arg(8)]-vasopressin (AVP) regulates fluid balance via V(2) receptors and glucose homeostasis through V(1A) and V(1B) receptors.
- Previous studies show V(1A) receptor deficiency causes hyperglycemia and V(1B) deficiency causes hypoglycemia.
- AVP V(1A)/V(1B) double-deficient mice exhibit impaired glucose tolerance.
Purpose of the Study:
- To clarify the role of the entire AVP/vasopressin receptor system in blood glucose regulation.
- To investigate the effect of AVP deficiency on glucose tolerance.
Main Methods:
- Oral glucose tolerance test (GTT) was performed on AVP-deficient homozygous Brattleboro (di/di) rats.
- Plasma glucose and insulin levels were measured during the GTT.
Main Results:
- Homozygous di/di rats showed lower plasma glucose and insulin levels compared to heterozygous di/+ rats during GTT.
- These findings suggest AVP deficiency leads to enhanced glucose tolerance.
Conclusions:
- AVP deficiency, by blocking all AVP/vasopressin receptors, results in enhanced glucose tolerance.
- The AVP/vasopressin receptor system significantly contributes to the regulation of blood glucose homeostasis.
