A Gpbar1-deficient mouse is constructed and it is examined whether or not Gpbar1 participates in the regulation of bile acid homeostasis and lipid metabolism. As a result, the total bile acid pool is decreased in the Gpbar1-deficient mouse without showing any change in the fecal bile acid level. A female Gpbar1-deficient mouse having been fed with a high fat feed shows a significant increase in body weight compared with a wild type mouse, which is caused by an increase in fat. These facts suggest that Gpbar1 contributes to the regulation of bile acid homeostasis and lipid metabolism.