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Hypoxia increases expression of selective facilitative glucose transporters (GLUT) and 2-deoxy-D-glucose uptake in human adipocytes.

Wood IS, Wang B, Lorente-Cebrián S, Trayhurn P - Biochem. Biophys. Res. Commun. (2007)

Bottom Line: 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.

View Article: PubMed Central - PubMed

Affiliation: Obesity Biology Unit, School of Clinical Sciences, University Clinical Departments, Royal Liverpool University Hospital, University of Liverpool, UK. i.s.wood@liverpool.ac.uk

ABSTRACT
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.

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Related in: MedlinePlus

Facilitative glucose transporter gene expression in human adipocytes in hypoxia. Adipocytes at day 14 (post-induction of differentiation) were exposed to 21% or 1% O2 for up to 24 h. Total RNA was isolated and GLUT gene family mRNAs quantified by real-time PCR. Results are mean values ± SE (n = 4), expressed as relative to the control group. (A) ‘Zen-Bio’ adipocytes; (B) SGBS adipocytes. Twenty-one percent of O2 (open bars); 1% O2 (shaded bars). ∗P < 0.05; ∗∗P < 0.01; ∗∗∗P < 0.001, compared to adipocytes in normoxia.
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fig1: Facilitative glucose transporter gene expression in human adipocytes in hypoxia. Adipocytes at day 14 (post-induction of differentiation) were exposed to 21% or 1% O2 for up to 24 h. Total RNA was isolated and GLUT gene family mRNAs quantified by real-time PCR. Results are mean values ± SE (n = 4), expressed as relative to the control group. (A) ‘Zen-Bio’ adipocytes; (B) SGBS adipocytes. Twenty-one percent of O2 (open bars); 1% O2 (shaded bars). ∗P < 0.05; ∗∗P < 0.01; ∗∗∗P < 0.001, compared to adipocytes in normoxia.

Mentions: Human adipocytes differentiated from preadipocytes (Zen-Bio) in culture were incubated in 21% or 1% O2 for 4, 8, and 24 h, and the levels of mRNA for specified GLUT gene family members assessed by real-time PCR. As shown in Fig. 1A, a significant increase (4-fold) was observed in the relative level of GLUT-1 mRNA by 4 h and at the subsequent time points. GLUT-1 mRNA level was highest at 24 h, with a 9.2-fold increase. When the cells were returned to 21% O2 (for 16 h) following exposure to 1% O2 for 8 h, GLUT-1 mRNA level returned to initial levels.


Hypoxia increases expression of selective facilitative glucose transporters (GLUT) and 2-deoxy-D-glucose uptake in human adipocytes.

Wood IS, Wang B, Lorente-Cebrián S, Trayhurn P - Biochem. Biophys. Res. Commun. (2007)

Facilitative glucose transporter gene expression in human adipocytes in hypoxia. Adipocytes at day 14 (post-induction of differentiation) were exposed to 21% or 1% O2 for up to 24 h. Total RNA was isolated and GLUT gene family mRNAs quantified by real-time PCR. Results are mean values ± SE (n = 4), expressed as relative to the control group. (A) ‘Zen-Bio’ adipocytes; (B) SGBS adipocytes. Twenty-one percent of O2 (open bars); 1% O2 (shaded bars). ∗P < 0.05; ∗∗P < 0.01; ∗∗∗P < 0.001, compared to adipocytes in normoxia.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC2211375&req=5

fig1: Facilitative glucose transporter gene expression in human adipocytes in hypoxia. Adipocytes at day 14 (post-induction of differentiation) were exposed to 21% or 1% O2 for up to 24 h. Total RNA was isolated and GLUT gene family mRNAs quantified by real-time PCR. Results are mean values ± SE (n = 4), expressed as relative to the control group. (A) ‘Zen-Bio’ adipocytes; (B) SGBS adipocytes. Twenty-one percent of O2 (open bars); 1% O2 (shaded bars). ∗P < 0.05; ∗∗P < 0.01; ∗∗∗P < 0.001, compared to adipocytes in normoxia.
Mentions: Human adipocytes differentiated from preadipocytes (Zen-Bio) in culture were incubated in 21% or 1% O2 for 4, 8, and 24 h, and the levels of mRNA for specified GLUT gene family members assessed by real-time PCR. As shown in Fig. 1A, a significant increase (4-fold) was observed in the relative level of GLUT-1 mRNA by 4 h and at the subsequent time points. GLUT-1 mRNA level was highest at 24 h, with a 9.2-fold increase. When the cells were returned to 21% O2 (for 16 h) following exposure to 1% O2 for 8 h, GLUT-1 mRNA level returned to initial levels.

Bottom Line: 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.

View Article: PubMed Central - PubMed

Affiliation: Obesity Biology Unit, School of Clinical Sciences, University Clinical Departments, Royal Liverpool University Hospital, University of Liverpool, UK. i.s.wood@liverpool.ac.uk

ABSTRACT
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.

Show MeSH
Related in: MedlinePlus