Linolenic acid transport in hamster intestinal cells is carrier-mediated.

The intestinal uptake of [1-14C]linolenic acid [18:3(n-3)], an essential fatty acid, was investigated in isolated hamster intestinal cells using a rapid filtration method and 20 mmol/L taurocholate as solubilizing agent. Under these conditions, the initial rate of alpha-linolenic acid uptake was not a linear function of external monomer concentrations in the range of 2 to 2250 nmol/L, but rather the transport system was characterized by saturation kinetics with Vmax = 11.37 nmol.mg protein-1.min-1 and Km = 382 nmol/L. Temperature and metabolic poisons (2,4-dinitrophenol, antimycin A) drastically decreased the initial rate of uptake, as did replacement of Na+. The presence of excess unlabeled alpha-linolenic acid in the incubation medium significantly inhibited the uptake of [1-14C]linolenic acid, whereas L-alanine and D-glucose had no effect. Other long-chain fatty acids (saturated or unsaturated), as well as cholesterol, inhibited the uptake of [1-14C]linolenic acid. We concluded that an active, carrier-mediated mechanism was involved in the intestinal transport of alpha-linolenic acid. Inhibition data are compatible with the hypothesis that intestinal uptake of alpha-linolenic acid is mediated by a carrier common to long-chain fatty acids.