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The influence of hydrazine, phenelzine and nialamide on gluconeogenesis and cell respiration in the perfused guinea‐pig liver
Author(s) -
HAECKEL R.,
OELLERICH M.
Publication year - 1977
Publication title -
european journal of clinical investigation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.164
H-Index - 107
eISSN - 1365-2362
pISSN - 0014-2972
DOI - 10.1111/j.1365-2362.1977.tb01625.x
Subject(s) - gluconeogenesis , nialamide , pyruvic acid , endocrinology , medicine , phenelzine , phosphoenolpyruvate carboxykinase , hydrazine (antidepressant) , pyruvate carboxylase , respiration , chemistry , biochemistry , metabolism , metabolite , hydrazone , biology , medicinal chemistry , monoamine oxidase , enzyme , botany
. Hydrazine (2 mmol/l) and phenelzine (0.5 mmol/l), which are known to produce hypoglycaemia, inhibit glucose formation from lactate in the perfused guinea‐pig liver. The hydrazone formed from pyruvate and phenelzine exerted the same effect at concentrations of only 0.05 mmol/l. It is suggested that the hydrazones are the substances which are effective. All these compounds inhibited pyruvate consumption and decreased CO 2 production by the perfused liver which, together with the pattern of hepatic metabolite concentrations, indicate that they diminish pyruvate metabolism. None of them influenced the activities in vitro of pyruvate carboxylase, phosphoenolpyruvate carboxykinase and pyruvate dehydrogenase. The hydrazone compound caused an increase of the ATP/ADP ratio at lower concentrations and an opposite effect above 0.5 mmol/l. Nialamide, another hydrazine derivative, also reduced hepatic gluconeogenesis but led to a marked decrease in the hepatic ATP/ADP ratio and liver cell respiration accompanied by a rise in the 3‐hydroxybutyrate/acetoacetate ratio.