Wood I Stuart, Wang Bohan, Lorente-Cebrián Silvia, Trayhurn Paul
Obesity Biology Unit, School of Clinical Sciences, University Clinical Departments, Royal Liverpool University Hospital, University of Liverpool, UK.
Biochem Biophys Res Commun. 2007 Sep 21;361(2):468-73. doi: 10.1016/j.bbrc.2007.07.032. Epub 2007 Jul 18.
Hypoxia modulates the production of key inflammation-related adipokines and may underlie adipose tissue dysfunction in obesity. Here we have examined the effects of hypoxia on glucose transport by human adipocytes. Exposure of adipocytes to hypoxia (1% O(2)) for up to 24 h resulted in increases in GLUT-1 (9.2-fold), GLUT-3 (9.6-fold peak at 8 h), and GLUT-5 (8.9-fold) mRNA level compared to adipocytes in normoxia (21% O(2)). In contrast, there was no change in GLUT-4, GLUT-10 or GLUT-12 expression. The rise in GLUT-1 mRNA was accompanied by a substantial increase in GLUT-1 protein (10-fold), but there was no change in GLUT-5; GLUT-3 protein was not detected. Functional studies with [(3)H]2-deoxy-D-glucose showed that hypoxia led to a stimulation of glucose transport (4.4-fold) which was blocked by cytochalasin B. These results indicate that hypoxia increases monosaccharide uptake capacity in human adipocytes; this may contribute to adipose tissue dysregulation in obesity.
缺氧调节关键炎症相关脂肪因子的产生，可能是肥胖中脂肪组织功能障碍的潜在原因。在此，我们研究了缺氧对人脂肪细胞葡萄糖转运的影响。与常氧（21% O₂）条件下的脂肪细胞相比，将脂肪细胞暴露于缺氧环境（1% O₂）长达24小时，导致GLUT-1（9.2倍）、GLUT-3（8小时时峰值为9.6倍）和GLUT-5（8.9倍）的mRNA水平升高。相比之下，GLUT-4、GLUT-10或GLUT-12的表达没有变化。GLUT-1 mRNA的升高伴随着GLUT-1蛋白的显著增加（10倍），但GLUT-5没有变化；未检测到GLUT-3蛋白。用[³H]2-脱氧-D-葡萄糖进行的功能研究表明，缺氧导致葡萄糖转运受到刺激（4.4倍），这被细胞松弛素B阻断。这些结果表明，缺氧增加了人脂肪细胞的单糖摄取能力；这可能导致肥胖中脂肪组织的调节异常。
