期刊
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
卷 361, 期 2, 页码 468-473出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.bbrc.2007.07.032
关键词
hypoxia; HIF-1 alpha; human adipocytes; GLUT1; GLUT3; GLUT5; adipokines; obesity; metabolic syndrome; glucose transport
资金
- Biotechnology and Biological Sciences Research Council [BB/C006364/1] Funding Source: Medline
- Biotechnology and Biological Sciences Research Council [BB/C006364/1] Funding Source: researchfish
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- I protein (10-fold), but there was no change in GLUT-5; GLUT-3 protein was not detected. Functional studies with [H-3]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. (c) 2007 Elsevier Inc. All rights reserved.
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