Effect of Insulin on Fatty Acid Uptake and Esterification in L-Cell Fibroblasts

We examined the effects of insulin on fatty acid uptake in L-cell fibroblasts, usingcis-parinaric acid to measure uptake rates in the absence of esterification and [3H]oleic acid to measure uptake rates in the presence of esterification. L-cells exhibited both high and low affinity insulin binding sites withKdof 23 nMand 220 nMand a cellular density of 1.4 and 6.8 × 105sites/cell, respectively. Insulin in the range 10−9to 10−7Msignificantly decreased both the initial rate and maximal extent ofcis-parinaric acid uptake by 24 to 30%. Insulin also reduced [3H]oleic acid uptake up to 35%, depending on insulin concentration and decreased the amount of fatty acid esterified into the phospholipids and neutral lipids by 28 and 70%, respectively. In contrast, glucagon or epinephrine stimulated both the initial rate and extent ofcis-parinaric acid uptake 18 and 25%, respectively. Because L-cells lack β-adrenergic receptors, the epinephrine effect was not the result of β-receptor stimulation. Hence, insulin altered not only fatty acid uptake, as determined bycis-parinaric and oleic acid uptake, but also altered the intracellular oleic acid esterification.