Insulin causes fatty acid transport protein translocation and enhanced fatty acid uptake in adipocytes
Insulin causes fatty acid transport protein translocation and enhanced fatty acid uptake in adipocytes
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DOI：
10.1016/s1534-5807(02)00143-0
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发表时间：
2002-04-01
影响因子：
11.8
通讯作者：
Lodish, HF
中科院分区：
文献类型：
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作者：
Stahl, A;Evans, JG;Lodish, HF
3 T3 L1脂肪细胞的脂肪酸摄取主要是转运蛋白介导的。在这里，我们表明，在3 T3 L1脂肪细胞分化，脂肪酸转运蛋白（FATPs）1和4的表达诱导。使用亚细胞膜分离和免疫荧光显微镜，我们证明，在脂肪细胞中，胰岛素诱导FATPs从细胞内核周区室质膜易位到质膜。在胰岛素治疗的几分钟内观察到这种易位，并通过长链脂肪酸（LCFA）摄取的增加而消除。相反，TNF-α治疗抑制基础和胰岛素诱导的LCFA摄取，并降低FATP 1和-4水平。因此，FATP活性的激素调节可能在能量稳态和代谢紊乱如2型糖尿病中起重要作用。
Fatty acid uptake into 3T3 L1 adipocytes is predominantly transporter mediated. Here we show that, during 3T3 L1 adipocyte differentiation, expression of fatty acid transport proteins (FATPs) 1 and 4 is induced. Using subcellular membrane fractionation and immunofluorescence microscopy, we demonstrate that, in adipocytes, insulin induces plasma membrane translocation of FATPs from an intracellular perinuclear compartment to the plasma membrane. This translocation was observed within minutes of insulin treatment and was paralleled by an increase in long chain fatty acid (LCFA) uptake. In contrast, treatment with TNF-alpha inhibited basal and insulin-induced LCFA uptake and reduced FATP1 and -4 levels. Thus, hormonal regulation of FATP activity may play an important role in energy homeostasis and metabolic disorders such as type 2 diabetes.