Abstract
Summary Biotin-deficient animals show a reduction in incorporation of pyruvate-214C into glucose with progressive onset of the deficiency. The oxidation and utilization of pyruvate is reduced by 50 per cent. The pyruvate carboxylase activity was greatly decreased whereas PEP carboxykinase activity was found to be slightly decreased in biotin deficiency. In vitro administration of biotin to biotin-deficient animals almost restored the pyruvate carboxylase activity and PEP carboxykinase activity was only slightly altered. In addition, it is observed that pyruvate carboxylase can be extracted from the mitochondria by homogenizing at room temperature and is quite stable under these conditions.

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