Add time:08/22/2019         Source:sciencedirect.com

Displacement of fatty acids or their CoA esters from the cytosolic fatty acid-binding-protein (FABP) by β-flavaspidic acid-N-methyl-glucaminate (flavaspidic acid) shifted the flow of lactate from the lipogenic to the gluconeogenic pathway in hepatocytes isolated from livers of fed rats. Analyses of radiolabel in products of 1 hour incubations utilizing 40 mM DL-sodium lactate (U-14C sodium lactate or 3H2O) as substrate showed fatty acid synthesis to be depressed in the presence of 5 mM flavaspidic acid to levels ranging to 28% of control. Glucose synthesis, on the other hand, rose to a level 809% of control, a rate approximately equivalent to the maximal rate of gluconeogenesis found in hepatocytes from diabetic rats. The production of ketone bodies was not influenced by flavaspidic acid whereas CO2 production decreased reflecting the diversion of the flow of lactate from the lipogenic to the gluconeogenic pathway.These results are presented in support of the hypothesis that unbound long-chain acyl CoA esters act as physiological effectors of the adenine nucleotide translocation and through this action, integrate lipogenic and gluconeogenic activities. Flavaspidic acid thus serves as a useful probe for studies of the role of long chain acyl CoA esters in the intracellular regulation of intermediary metabolism and of the modulation exerted by the FABP.

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