Hypoxia increases expression of selective facilitative glucose transporters (GLUT) and 2-deoxy-D-glucose uptake in human adipocytes.
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.
Obesity Biology Unit, School of Clinical Sciences, University Clinical Departments, Royal Liverpool University Hospital, University of Liverpool, UK. i.s.wood@liverpool.ac.uk
I Stuart
IS
Wood
Bohan
B
Wang
Silvia
S
Lorente-Cebrián
Paul
P
Trayhurn
D017667:Adipocytes / Q000166:cytology* / Q000378:metabolism*; D000328:Adult; D015687:Cell Hypoxia; D003847:Deoxyglucose / Q000378:metabolism*; D005260:Female; D005786:Gene Expression Regulation; D051246:Glucose Transport Proteins, Facilitative / Q000235:genetics* / Q000378:metabolism*; D006801:Humans; D015151:Immunoblotting
D051246:Glucose Transport Proteins, Facilitative; D003847:Deoxyglucose