Linoleic acid uptake by isolated enterocytes: Influence of α‐linolenic acid on absorption

In a previous study we showed that intestinal uptake of α‐linolenic acid (18∶3n−3) was carrier‐mediated and we suggested that a plasma membrane fatty acid protein was involved in the transport of long‐chain fatty acids. To further test this hypothesis, the mechanism of linoleic acid (18∶2n−6) uptake by isolated intestinal cells was examined using a rapid filtration method and 20 mM sodium taurocholate as solubilizing agent. Under these experimental conditions transport of [1‐14C]linoleic acid monomers in the concentration range of 2 to 2220 nM was saturable with a Vm of 5.1±0.6 nmol/mg protein/min and a Km of 183±7 nM. Experiments carried out in the presence of metabolic inhibitors, such as 2,4‐dinitrophenol and antimycin A, suggested that an active, carriermediated mechanism was involved in the intestinal uptake of this essential fatty acid. The addition of excess unlabeled linoleic acid to the incubation medium led to a 89% decrease in the uptake of [1‐14C]linoleic acid, whiled‐glucose did not compete for transport into the cell. Other long‐chain polyunsaturated fatty acids added to the incubation mixture inhibited linoleic acid uptake by more than 80%. The presence of α‐linolenic acid (18∶3n−3) in the incubation medium caused the competitive inhibition (Ki=353 nM) of linoleic acid uptake. The data are compatible with the hypothesis that intestinal uptake of both linoleic, and α‐linolenic acid is mediated by a membrane carrier common to long‐chain fatty acids.