The Effects of 2‐Ethylcitrate and Tricarballylate on Citrate Transport in Rat Liver Mitochondria and Fatty Acid Synthesis in Rat White Adipose Tissue

TLDR: Neither 2-ethylcitrate nor tricarballylate at low concentrations (< 10 mM) were found to inhibit fatty acid synthesis with pyruvate as precursor in rat white adipose tissue but both were potent inhibitors of fatty acids synthesis with glucose as precursor.

Abstract: 2-Ethylcitrate and propane 1,2,3 tricarboxylic acid (tricarballylate) were found to be inhibitors of the citrate transporting system as monitored by cis-aconitate and isocitrate oxidation. Kinetic data showed the inhibitions to be competitive with tricarboxylate anion. When the exchange of intramitochondrial [14C]citrate with added extramitochondrial citrate or L-malate was measured at low temperatures, 2-ethylcitrate and 2-propylcitrate were found to be good inhibitors, while tricarballylate did not inhibit and in fact was found to be a good substrate for exchange on the transporting system. Neither 2-ethylcitrate nor tricarballylate at low concentrations (< 10 mM) were found to inhibit fatty acid synthesis with pyruvate as precursor in rat white adipose tissue but both were potent inhibitors of fatty acid synthesis with glucose as precursor. The implications of these findings are discussed.