Sfeir Z, Ibrahimi A, Amri E, Grimaldi P, Abumrad N
Department of Physiology and Biophysics, State University of New York at Stony Brook, 11733, USA.
Prostaglandins Leukot Essent Fatty Acids. 1997 Jul;57(1):17-21. doi: 10.1016/s0952-3278(97)90487-7.
Much biochemical evidence has implicated rat adipocyte CD36 (FAT) in membrane binding and transport of long-chain fatty acids (FA). Expression of the mRNA favored tissues with active FA metabolism and was upregulated in vivo with diabetes and with high fat feeding. In culture, CD36 mRNA was a strong marker of preadipocyte differentiation and was modulated by the same factors effective on mRNAs coding for other proteins involved in FA metabolism. In preadipocytes, long-chain FA or 2-bromopalmitate but not short-chain FA strongly induced CD36 mRNA within 8 h to an optimum within 24 h. Removal of the FA resulted in a decay of CD36 mRNA with a half life of about 12 h. In differentiated adipocytes, levels of CD36 mRNA were downregulated by the 3': 5'-cyclic adenosine monophosphate, cAMP, analog, 8-(4-chlorophenylthio) adenosine, 8-CPT, at concentrations of 1-100 microM. The effect, observed within 6 h, was optimal after 18 h and independent of the action of 8-CPT to mobilize FA. Regulation of CD36 expression by factors effective on expression of other proteins implicated in FA metabolism is consistent with its role in membrane FA transport.
许多生化证据表明，大鼠脂肪细胞CD36（FAT）参与长链脂肪酸（FA）的膜结合和转运。mRNA的表达在脂肪酸代谢活跃的组织中更为常见，并且在糖尿病和高脂喂养的体内情况下会上调。在培养过程中，CD36 mRNA是前脂肪细胞分化的一个重要标志物，并且受到与调控其他参与脂肪酸代谢的蛋白质的mRNA相同的因素的调节。在前脂肪细胞中，长链脂肪酸或2-溴棕榈酸酯而非短链脂肪酸在8小时内可强烈诱导CD36 mRNA表达，并在24小时内达到最佳水平。去除脂肪酸后，CD36 mRNA会衰减，半衰期约为12小时。在分化的脂肪细胞中，3':5'-环磷酸腺苷（cAMP）类似物8-（4-氯苯硫基）腺苷（8-CPT）在浓度为1-100微摩尔时会下调CD36 mRNA的水平。这种作用在6小时内即可观察到，18小时后达到最佳效果，且与8-CPT动员脂肪酸的作用无关。对参与脂肪酸代谢的其他蛋白质表达有影响的因素对CD36表达的调节，与其在膜脂肪酸转运中的作用是一致的。
