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大西洋鲑(Salmo salar)中跨膜脂肪酸转运蛋白的体内和体外胰岛素及禁食调控。

In vivo and in vitro insulin and fasting control of the transmembrane fatty acid transport proteins in Atlantic salmon (Salmo salar).

机构信息

Departament de Fisiologia, Facultat de Biologia, Universitat de Barcelona, Spain, Av. Diagonal 645, E-08028 Barcelona, Spain.

出版信息

Am J Physiol Regul Integr Comp Physiol. 2011 Oct;301(4):R947-57. doi: 10.1152/ajpregu.00289.2011. Epub 2011 Jul 20.

DOI:10.1152/ajpregu.00289.2011
PMID:21775646
Abstract

We have examined the nutritional and insulin regulation of the mRNA expression of transmembrane fatty acid (FA) transporters [FA transport protein-1 (FATP1) and CD36] together with the lipoprotein lipase (LPL), the cytosolic FA carrier FA binding protein (FABP3), and mitochondrial FA-CoA and -carnitine palmitoyl transferase carriers (CPT)1 and -2 in Atlantic salmon tissues and myocyte cell culture. Two weeks of fasting diminished FATP1, CD36, and LPL in adipose tissue, suggesting a reduction in FA uptake, while FABP3 increased in liver, probably enhancing the transport of FA to the mitochondria. Insulin injection decreased FATP1 and CD36 in white and red muscles, while both transporters were upregulated in the adipose tissue in agreement with the role of insulin-inhibiting muscle FA oxidation and stimulating adipose fat stores. Serum deprivation of 48 h in Atlantic salmon myotubes increased FATP1, FABP3, and CPT-2, while CPT-1 was diminished. In myotubes, insulin induced FATP1 expression but decreased CD36, FABP3, and LPL, suggesting that FATP1 could be more involved in the insulin-stimulated FA uptake. Insulin increased the FA uptake in myotubes mediated, at least in part, through the relocation of FATP1 protein to the plasma membrane. Overall, Atlantic salmon FA transporters are regulated by fasting and insulin on in vivo and in vitro models.

摘要

我们研究了跨膜脂肪酸 (FA) 转运蛋白 [FA 转运蛋白-1 (FATP1) 和 CD36] 的 mRNA 表达,以及脂蛋白脂肪酶 (LPL)、细胞质 FA 载体 FA 结合蛋白 (FABP3) 和线粒体 FA-CoA 和 -肉碱棕榈酰转移酶载体 (CPT)1 和 -2 的营养和胰岛素调节,在大西洋三文鱼组织和肌细胞培养物中。两周的禁食减少了脂肪组织中的 FATP1、CD36 和 LPL,表明 FA 摄取减少,而肝脏中的 FABP3 增加,可能增强 FA 向线粒体的转运。胰岛素注射减少了白色和红色肌肉中的 FATP1 和 CD36,而这两种转运蛋白在脂肪组织中均上调,这与胰岛素抑制肌肉 FA 氧化和刺激脂肪储存的作用一致。48 小时剥夺大西洋三文鱼肌管中的血清增加了 FATP1、FABP3 和 CPT-2,而 CPT-1 减少。在肌管中,胰岛素诱导 FATP1 的表达,但减少 CD36、FABP3 和 LPL,表明 FATP1 可能更多地参与胰岛素刺激的 FA 摄取。胰岛素增加了肌管中的 FA 摄取,至少部分是通过 FATP1 蛋白向质膜的重新定位介导的。总体而言,大西洋三文鱼 FA 转运蛋白受体内和体外模型的禁食和胰岛素调节。

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