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Eur J Pharmacol. 2009 Jan 14;602(2-3):455-61. doi: 10.1016/j.ejphar.2008.11.043. Epub 2008 Dec 3.

Altered lipid metabolism in vasopressin V1B receptor-deficient mice.

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Department of Pharmacology, National Research Institute for Child Health and Development, Tokyo, Japan.


We previously reported that insulin sensitivity was increased in vasopressin V(1B) receptor-deficient (V(1B)R(-/-)) mice. Here, we investigate the lipid metabolism in V(1B)R(-/-) mice. Despite having lower body weight, V(1B)R(-/-) mice had significantly greater fat weight of the epididymal white adipose tissue than V(1B)R(+/+) mice. Glycerol production and beta-oxidation were suppressed in V(1B)R(-/-) mice under a fasting condition, and isoproterenol-stimulated lipolysis in differentiated adipocytes was significantly decreased in V(1B)R(-/-) mice. These results indicated that lipolysis was inhibited in V(1B)R(-/-) mice. On the other hand, lipogenesis was promoted by the increased metabolism from glucose to lipid. Furthermore, our in vivo and in vitro analyses showed that the secretion of adiponectin was increased in V(1B)R(-/-) mice, while the serum leptin level was lower in V(1B)R(-/-) mice. These findings indicated that the insulin sensitivity and lipid metabolism were altered in V(1B)R(-/-) mice and that the increased insulin sensitivity could contribute to the suppressed lipolysis and enhanced lipogenesis, which consequently resulted in the increased fat weight in V(1B)R(-/-) mice.

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