Sodium-dependent succinate transport by isolated chick intestinal cells.

Isolated chick intestinal epithelial cells take up succinate by a Na(+)-coupled transport system similar in some characteristics to those described for renal epithelium. The transport system exhibits a hyperbolic dependence on succinate concentration but a sigmoidal dependence on Na+ concentration. Best nonlinear fit of the Na+ dependence data to the Hill equation indicates a Michaelis constant for half-maximal transport rate (Km) for Na+ of approximately 20 mM, a maximal transport rate (Vmax) of 1.1 nmol succinate.min-1.mg protein-1, and a Hill coefficient of 2.5. Nearly equivalent fit was obtained with trial Hill coefficients down to 2.0. The data for succinate dependence indicated a Km of 25 microM and Vmax of 1.05 nmol.min-1.mg protein-1. The kinetic parameters indicate a higher affinity, lower capacity system than for succinate transport in the renal brush-border system. Thiocyanate-induced diffusion potentials cause no change in Na(+)-dependent succinate influx despite pronounced effects on the influx of tetraphenylphosphonium and on Na(+)-dependent alpha-methylglucoside (AMG) and alanine uptake. Several other dicarboxylic and tricarboxylic metabolic intermediates (but not the dicarboxylic amino acids) compete with succinate for uptake via the transport system. The data are consistent with the likelihood that these cells have a succinate transport system with a 2Na+:1succinate stoichiometry per transport cycle. The system catalyzes no net charge transfer and is therefore different from the potential-responsive succinate transporter described for renal tissue.