Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: EC:4.1.1.32 (
phosphoenolpyruvate carboxykinase
)
4,204
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
The inhibitory effects of metabolites of L-tryptophan on gluconeo-genesis in rat renal cortex has been established. 1. Glucose production was inhibitied by quinolinate in vitro. The inhibition is due to the decreased
phosphoenolpyruvate carboxykinase
activity. As suggested for purified enzyme systems, quinolinate seems to exert its action in tissue slices by chelating divalent metal ions. The minimum effective extracellular concentration of the inhibitor was 5 X 10(-5) M with pyruvate as a precursor for gluconeo-genesis. 2. The effect of
3-hydroxyanthranilate
is stronger (minimal effective concentration 10(-5) M) than that of quinolinate.
3-Hydroxyanthranilate
may be effective in its original form and/or as a dimer degrandation product. The compound(s) exert a second effect in addition to blocking the
phosphoenolpyruvate carboxykinase
. This block is attained by conversion of
3-hydroxyanthranilate
to quinolinate. The non-quinolinate mediated effect may be due to a reduced ATP regeneration. 3. It is suggested that kidney cortex responds sensitively to disturbances in ATP metabolism by reduction of glucose synthesis, when it is not the result of blocked formation of phosphoenolpyruvate.
...
PMID:Inhibition of gluconeogenesis in rat renal cortex slices by metabolites of L-tryptophan in vitro. 115 21