Murphy E J, Prows D R, Jefferson J R, Incerpi S, Hertelendy Z I, Heyliger C E, Schroeder F
Department of Physiology and Pharmacology, Texas A&M University, TVMC, College Station 77843-4466, USA.
Arch Biochem Biophys. 1996 Nov 15;335(2):267-72. doi: 10.1006/abbi.1996.0507.
We examined the effects of insulin on fatty acid uptake in L-cell fibroblasts, using cis-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 with Kd of 23 nM and 220 nM and a cellular density of 1.4 and 6.8 x 10(5) sites/cell, respectively. Insulin in the range 10(-9) to 10(-7) M significantly decreased both the initial rate and maximal extent of cis-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 of cis-parinaric acid uptake 18 and 25%, respectively. Because L-cells lack P-adrenergic receptors, the epinephrine effect was not the result of P-receptor stimulation. Hence, insulin altered not only fatty acid uptake, as determined by cis-parinaric and oleic acid uptake, but also altered the intracellular oleic acid esterification.
我们使用顺式十八碳四烯酸来测量在无酯化作用时的摄取速率，并使用[3H]油酸来测量在有酯化作用时的摄取速率，研究了胰岛素对L细胞成纤维细胞中脂肪酸摄取的影响。L细胞表现出高亲和力和低亲和力的胰岛素结合位点，其解离常数（Kd）分别为23 nM和220 nM，细胞密度分别为1.4和6.8×10(5)个位点/细胞。10(-9)至10(-7) M范围内的胰岛素可使顺式十八碳四烯酸摄取的初始速率和最大程度显著降低24%至30%。胰岛素还可使[3H]油酸摄取降低达35%，具体取决于胰岛素浓度，并使酯化到磷脂和中性脂质中的脂肪酸量分别减少28%和70%。相比之下，胰高血糖素或肾上腺素可分别刺激顺式十八碳四烯酸摄取的初始速率和程度增加18%和25%。由于L细胞缺乏β-肾上腺素能受体，肾上腺素的作用并非β-受体刺激的结果。因此，胰岛素不仅改变了由顺式十八碳四烯酸和油酸摄取所确定的脂肪酸摄取，还改变了细胞内油酸的酯化作用。
