Whether cellular oleate uptake is Na+ coupled remains controversial. Our present studies document that hepatocellular [H-3]oleate uptake is unaltered by isosmotic substitution of Na+ with K+, Li+, or sucrose in Hanks' HEPES buffer. In parallel studies Na-22+ uptake was significantly (P < 0.02) increased by concentrations of alanine that yielded [H-3]alanine uptakes > 24% of basal Na-22+ uptake when both were expressed as nanomoles per minute per 10(6) hepatocytes. Although [H-3]glutamine uptake exceeded this threshold, maximal specific [H-3]taurocholate uptake did not. Consistent with the observations with alanine, addition of glutamine, but not taurocholate, to the incubations resulted in a significant increase in Na-22+ uptake. The ionophore monensin increased uptake of Na-22+ under all conditions. Both in the absence and in the presence of HCO3- (4 and 25 mM), specific [H-3]oleate uptake was sufficient to elicit a readily detectable effect on Na-22+ uptake, if Na+ and oleate were cotransported. However, addition of 1 mM oleate did not affect Na-22+ uptake in the absence of HCO3- (5.4 +/- 0.6 vs. control 5.4 +/- 0.4 nmol . min-1 . 10(6) cells-1) as well as in the presence of 4 mM HCO3- (10.4 +/- 1.8 vs. control 9.9 +/- 1.1) and 25 mM HCO3- (10 +/- 1.3 vs. control 10.8 +/- 0.5). These data indicate that the predominant component of hepatocellular oleate uptake is not directly associated with Na+ influx. They do not exclude, however, a more complex or indirect link.
