作者: J R Williamson , R Scholz , E T Browning , R G Thurman , M H Fukami
DOI: 10.1016/S0021-9258(18)94307-3
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摘要: Abstract In the present study, ethanol oxidation by perfused rat liver has been used to investigate interrelationships between pathways of glucose metabolism, fatty acid oxidation, and citric cycle. absence exogenous acids, production from alanine was stimulated 2-fold 10 mm ethanol, whereas, in presence 1 oleate, caused an inhibition net production. Measurements rates utilization acetate formation showed that over 80% metabolized converted acetate. The increased rate generation reducing equivalents cytosol during oxidation-reduction state pyridine nucleotides both intra- extramitochondrial compartments. This fact established analyses tissue content substrate couple ratios, directly surface fluorometry. Changes flavin nucleotide fluorescence intensity transfer mitochondria very rapid. Analyses intermediates gluconeogenic pathway livers acids indicated activational site at glyceraldehyde-3-P dehydrogenase step upon addition. stimulatory effect on gluconeogenesis alanine, therefore, results availability NADH cytosol. On other hand, when added inhibitory observed fructose-1, 6-di-P fructose-6-P. Measurement levels known modifiers phosphofructokinase fructose diphosphate phosphatase this primarily deinhibition resulting a fall citrate content. Oxidation produced metabolism inhibited activity Sites were identified synthase iso-citrate steps. relative strengths interactions these sites dependent β oxidation. It is proposed coordinated isocitrate mediated reduction intramitochondrial nucleotides.