Abstract
Especially during the later stages of pregnancy a fair amount of lactate is transported via the placenta from the foetue to the mother. This extra lactate has to be oxidized by the mother or converted to glucose by gluconeogenesis. The oxidation of pyruvate is controlled by the pyruvate dehydrogenase(PDH) by phosphorylation and dephosphorylation. The phosphorylated enayme is inactive. Thiamine diphosphate (TPP) inhibits the phosphorylation. It was found the mitochondria of the liver of pregnant rats contain less TPP than controls. The TPP content of fetal rat liver mitochondria was found to be in between that of controls and pregnant rats. The mitochondrial TPP content corresponded to the degree of inhibition of mitochondrial PDH by ATP. Intraperitoneal injection of thiamine to pregnant rats resulted in an increase in TPP content of the fetal rat liver mitochondria, but hardly of the liver mitocondria of the mother animal. These results can be interpreted as a physiological control mechanism of the TPP level on PDH activity. The increased supply of lactate from the foetus to the mother calls for a higher rate of gluconeogenesis by the mother. Pyruvate oxidation must than be shut down to prevent waste of substrate.
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Hoeketra, D., Berger, R. & Hommes, F. CONTROL OF PYRUVATE OXIDATION IN FETAL AND MATERNAL TISSUE BY THE THIAMINE LEVEL. Pediatr Res 8, 132 (1974). https://doi.org/10.1203/00006450-197402000-00038
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DOI: https://doi.org/10.1203/00006450-197402000-00038