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Transplacental transport and tissue distribution of biotin in mice at midgestation
Author(s) -
Taniguchi Ayumi,
Watanabe Toshiaki
Publication year - 2008
Publication title -
congenital anomalies
Language(s) - English
Resource type - Journals
eISSN - 1741-4520
pISSN - 0914-3505
DOI - 10.1111/j.1741-4520.2008.00179.x
Subject(s) - biotin , biotin deficiency , fetus , biology , morphogenesis , endocrinology , vitamin , pyruvate carboxylase , medicine , biochemistry , pregnancy , enzyme , gene , genetics
Biotin is a water‐soluble vitamin which functions as a coenzyme of carboxylases in glucose and amino acid metabolism and fatty acid synthesis. Biotin is also essential for maintaining reproductive function. Biotin deficiency during gestation induces cleft palate, micrognathia and limb hypoplasia in mouse fetuses at near term. Maternal biotin deficiency is severely tetatogenic in mammals. However, the relationship between abnormal morphogenesis and biotin deficiency 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. Pregnant mice were given either a biotin‐deficient or biotin‐supplemented diet, and biotin and biotinidase activity were determined in dams and fetuses. It became evident that biotin was supplied from dams to growing embryos during morphogenesis. In particular, a large amount of biotin was transported to palates and mandibles on days 12–15 of gestation. The transportation of biotin to fetuses differed among fetal growth periods and organs. These results suggest that biotin is an essential nutrient and may play an important role in embryonic growth.