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METABOLISM OF GLUCOSE AND FREE AMINO ACIDS IN BRAIN, STUDIED WITH 14 C‐LABELLED GLUCOSE AND BUTYRATE IN RATS INTOXICATED WITH CARBON DISULPHIDE
Author(s) -
Tarkowski S.,
Cremer Jill E.
Publication year - 1972
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.1972.tb01322.x
Subject(s) - metabolism , glutamine , amino acid , butyrate , glutamate receptor , biochemistry , chemistry , compartment (ship) , carbohydrate metabolism , biology , medicine , fermentation , oceanography , receptor , geology
— The effect of 15 h continuous exposure to CS 2 on the metaboliam of glucose and free amino acids in the brain of rats was studied. CS 2 caused a moderate hypoglycaemia. There were also changes in the amounts of some amino acids in the brain. Glutamate and γ‐aminobutyrate were lower whereas glutamine was markedly increased. Comparative studies in vivo of the metabolism of [2‐ 14 C]glucose and [1‐ 14 C]butyrate indicated that CS 2 did not affect glycolysis or the incorporation of 14 C from glucose into amino acids except into γ‐aminobutyrate which was reduced. Contrary to the findings with [ 14 C]glucose, CS 2 provoked distinct changes in the labelling of amino acids when [ 14 C]butyrate was the precursor. The most notable change was a markedly increased incorporation of 14 C into glutamine. Based on the two‐compartment model of brain glutamate the experimental findings indicated that CS 2 affected metabolism associated with the ‘small’ pool of glutamate but had a minimal effect on metabolism associated with the ‘large’ glutamate pool. The possibility is suggested that the changes observed involved an increased rate of ammonia removal. The low incorporation of 14 C into γ‐aminobutyrate from either precursor is consistent with other evidence showing that CS 2 interferes with pyridoxal phosphate‐dependent enzymes.