Study on Teratogenicity of Biotin Deficiency in Mice at Midgestation

抄録

It is known that biotin is intrinsic for maintaining reproductive function. Biotin deficiency induces both external and skeletal malformations in the embryos of fowl, and maternal biotin deficiency is severely teratogenic in mammals. In mice, maternal biotin deficiency results in cleft palate, micrognathia and limb hypoplasia. However, the relationship between morphogenesis and biotin is not sufficiently clear. This study was conducted to elucidate the mechanism of biotin transport from dams to embryos and the nutritional roles of biotin in ICR mice. It became obvious that biotin was supplied from dams growing embryos during morphogenesis. In particular, a large amount of biotin was transported to palates and mandibles on days 12-15 of gestation. In fetuses, the transportation of biotin to embryos differed among embryonic growth periods and organs, and biotin may play a principal role in the formation of tissues and organs.

These results suggest that biotin is an essential nutrient and may play an important role in reproductive performance.