Beta-alanyl-L-histidinato zinc prevents skeletal unloading-induced disorder of bone metabolism in rats.

The effect of a new zinc compound beta-alanyl-L-histidinato zinc (AHZ) on the disorder of bone metabolism caused by skeletal unloading was investigated. Skeletal unloading was designed using the model of hind-limb hang in rats. Skeletal unloading for up to 4 days caused a remarkable decrease of zinc content, alkaline phosphatase activity, and DNA content in the femoral diaphysis of rats. Oral administration of AHZ (2.5, 5.0, and 10.0 mg/100 g) caused a significant increase in zinc, DNA, and calcium contents in the femoral diaphysis of rats with the skeletal unloading. Bone alkaline phosphatase activity was significantly increased by doses of 5.0 and 10.0 mg/100 g. These results clearly indicate that skeletal unloading-induced disorder of bone metabolism is prevented by the oral administration of AHZ. AHZ may be useful as a therapeutic tool in bone disorder.