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Control of gluconeogenesis in biotin-deficient rat liver

Authors
Journal
Archives of Biochemistry and Biophysics
0003-9861
Publisher
Elsevier
Publication Date
Volume
129
Issue
1
Identifiers
DOI: 10.1016/0003-9861(69)90182-9

Abstract

Abstract Incorporation of gluconeogenic precursors such as l-alanine-U- 14C, l-aspartate-U- 14C, succinate-1,4- 14C, NaH 14CO 3 and glycerol-U- 14C into blood glucose and liver glycogen was studied in control and pair-fed biotin-deficient rats. It was observed that only glycerol-U- 14C was utilized equally efficiently by control and deficient animals for glucose synthesis. A study of the levels of gluconeogenic intermediates, as well as the levels of reduced and oxidized forms of pyridine nucleotides in livers of fasted control and deficient animals, indicated two sites of control of gluconeogenesis in biotin deficiency: at the pyruvate carboxylase step and at the glyceraldehyde-3-phosphate dehydrogenase step. Under these conditions, abnormally large amounts of lactate were excreted in the urine of biotin-deficient animals.

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