Abstract
Extract: The rate of oxidation to respiratory CO2 of both carbon 1 of propionate and carbon 1 of glycine was decreased significantly in vitamin B12-deficient rats, to 50% and 82% of the control rate, respectively. The activity of the glycine synthase system was reduced during vitamin B12 deficiency to 25% of control activity. Serine hydroxymethyltransferase activity was similar for vitamin B12-deficient and control rats. Plasma glycine concentration in vitamin B12-deficient rats (253 ± 16 nmol/ml) did not differ significantly from that of control rats (226 ± 12 nmol/ml). Propionate oxidation was significantly impaired in biotin-deflcient rats. However, this impairment, to 66% of the control rate, was not as large as that generated by vitamin B12 deficiency. In contrast to the result obtained in vitamin B12-deficient animals, no significant decrease in glycine oxidation could be demonstrated in biotin-deficient animals Plasma glycine concentration of fasted biotin-deficient rats (339 ± 26 nmol/ml) did not differ significantly from that of their controls (371 ± 32 nmol/ml).
Speculation: Activity of the glycine synthase system is reduced in both the ketotic and nonketotic forms of hyperglycinemia. The decrease in glycine synthase system activity in vitamin B12-deficient rats may be generated by a mechanism similar to that in ketotic hyperglycinemia, and therefore vitamin B12-deficient rats may be useful to study this mechanism.
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Rowley, B., Brothers, V. & Gerritsen, T. The Vitamin B12-deficient Rat as a Possible Model of Ketotic Hyperglycinemia. Pediatr Res 9, 782–786 (1975). https://doi.org/10.1203/00006450-197510000-00007
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DOI: https://doi.org/10.1203/00006450-197510000-00007