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Inhibition of glucose phosphorylation by fatty acids in the perfused rat heart
Author(s) -
Chatham John,
Gilbert Hiram.F.,
Radda George K.
Publication year - 1988
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/0014-5793(88)80529-5
Subject(s) - glycolysis , dihydroxyacetone phosphate , glyceraldehyde , biochemistry , iodoacetic acid , glycogenolysis , butyrate , fructose , chemistry , dihydroxyacetone , glyceraldehyde 3 phosphate dehydrogenase , flux (metallurgy) , sugar phosphates , phosphorylation , dhap , dehydrogenase , glycogen , phosphate , metabolism , glycerol , enzyme , organic chemistry , fermentation
The flux of glucose entering the glycolytic pathway under various metabolic conditions has been indirectly monitored in the Langendorff perfused rat heart using 31 P‐NMR spectroscopy. By totally inhibiting (>95%) glyceraldehyde‐3‐phos‐phate dehydrogenase with low concentrations of iodoacetic acid (0.2 mM) in the perfusion medium, active glycolysis results in the accumulation of sugar phosphate species (fructose 1,6‐bisphosphate, dihydroxyacetone phosphate, and glyceraldehyde 3‐phosphate) which can be observed in the 31 P‐NMR spectrum. Using this technique, it has been shown that butyrate (10 mM) in the perfusion medium decreases the flux through the initial steps of the glycolytic pathway by at least 6‐fold and that both glucose phosphorylation and glycogenolysis are inhibited. Upon total global ischemia in the presence of both glucose and butyrate, the glycolysis rate is stimulated approx. 100‐fold.