Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
2534536 | European Journal of Pharmacology | 2009 | 7 Pages |
We previously reported that insulin sensitivity was increased in vasopressin V1B receptor-deficient (V1BR−/−) mice. Here, we investigate the lipid metabolism in V1BR−/− mice. Despite having lower body weight, V1BR−/− mice had significantly greater fat weight of the epididymal white adipose tissue than V1BR+/+ mice. Glycerol production and β-oxidation were suppressed in V1BR−/− mice under a fasting condition, and isoproterenol-stimulated lipolysis in differentiated adipocytes was significantly decreased in V1BR−/− mice. These results indicated that lipolysis was inhibited in V1BR−/− 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 V1BR−/− mice, while the serum leptin level was lower in V1BR−/− mice. These findings indicated that the insulin sensitivity and lipid metabolism were altered in V1BR−/− 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 V1BR−/− mice.