The relative specific activities of the respiratory CO2 deriving from the metabolism of [14C]glutamate, and [14C]aspartate in the presence and absence of non-radioactive glucose, and of [14C]glucose in the presence and absence of non-radioactive glutamate and aspartate in slices of rat brain cortex were determined. The values for glutamate and aspartate in the absence of glucose were 0·4 and 0·3 respectively, showing that 30 to 40% of the respiratory CO2 derived from these amino-acids. Aspartate, in contra-distinction to glutamate, does not increase the rate of oxygen of brain tissue above that due to endogenous substrates; yet the determination of the specific activity of the respiratory CO2 shows that this amino-acid too is readily oxidized by this tissue, replacing about a third of the endogenous sources of respiratory CO2. The addition of non-radioactive glucose as a co-substrate considerably stimulated the rate of oxygen uptake by brain tissue both in the presence of glutamate as well as aspartate, yet did not affect the specific activity of the respiratory CO2, indicating that glucose stimulated the oxidation of the amino-acids to the same extent as the oxidation of glucose itself or other non-amino acid substrates was increased. The addition of non-radioactive glutamate or aspartate to [14C]glucose resulted in a considerable decrease of the relative specific activity of the respiratory CO2, without affecting the rate of respiration, indicating that the oxidation of amino-acids replaced that of glucose, i.e. in this sense the amino-acids were preferentially oxidized. These results indicate that in the pattern of the oxidative processes of brain cortical tissue the oxidation of amino-acids plays an important part.
No takes yet. Share an insight, caveat, or question.
Chain et al. (1962) studied this question.
Synapse has enriched 2 closely related papers on similar clinical questions. Consider them for comparative context: