Prostaglandin F 2alpha enhances glucose consumption through neither adipocyte differentiation nor GLUT1 expression in 3T3-L1 cells
Arachidonic acid (AA) at 0.2 mM enhances glucose uptake through increased levels of glucose transporter (GLUT) 1 protein in 3T3-L1 adipocytes. Since AA is a precursor of prostaglandins (PGs), we investigated the effect of PGs on glucose consumption in 3T3-L1 cells. Among several PGs, only prostaglan...
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Published in | Cellular signalling Vol. 13; no. 2; pp. 105 - 109 |
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Main Authors | , , , |
Format | Journal Article |
Language | English |
Published |
Elsevier Inc
2001
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Subjects | |
Online Access | Get full text |
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Summary: | Arachidonic acid (AA) at 0.2 mM enhances glucose uptake through increased levels of glucose transporter (GLUT) 1 protein in 3T3-L1 adipocytes. Since AA is a precursor of prostaglandins (PGs), we investigated the effect of PGs on glucose consumption in 3T3-L1 cells. Among several PGs, only prostaglandin F
2alpha (PGF
2alpha) enhanced glucose consumption in 3T3-L1 cells treated with dexamethasone (DEX), 3-isobutyl-1-methyl-xanthine (IBMX), and insulin. To study the mechanism of PGF
2alpha-enhanced glucose consumption, we investigated the effect of PGF
2alpha on glycerol-3-phosphate dehydrogenase (GPDH) activity, triglycerides (TGs) content, and the expression of GLUT1 protein. PGF
2alpha suppressed GPDH activity and did not increase the expression of GLUT1 protein in 3T3-L1 cells treated with DEX, IBMX, and insulin. These results suggest that AA-stimulated glucose uptake is not through the effect of PGF
2alpha. Our results indicate that PGF
2alpha is a unique regulator of adipocyte differentiation (suppression) and glucose consumption (enhancement) in 3T3-L1 cells. |
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ISSN: | 0898-6568 1873-3913 |
DOI: | 10.1016/S0898-6568(00)00137-6 |