Prostaglandin F 2α increases glucose transport in 3T3-L1 adipocytes through enhanced GLUT1 expression by a protein kinase C-dependent pathway

Abstract

The effect of prostaglandin F 2α (PGF 2α) on glucose transport in differentiated 3T3-L1 adipocytes was examined. Whereas PGF 2α had little influence on insulin-stimulated 2-deoxyglucose uptake, it increased basal glucose uptake in a time- and dose-dependent manner, reaching maximum at approximately 8 h. The long-term effect of PGF 2α on glucose transport was inhibited by both cycloheximide and actinomycin D. In concord, while the content of GLUT4 protein was not altered, immunoblot and Northern blot analyses revealed that both GLUT1 protein and mRNA levels were increased by exposure of cells to PGF 2α. The effect of PGF 2α on glucose uptake was inhibited by GF109203X, a selective protein kinase C (PKC) inhibitor. In addition, in cells depleted of diacylglycerol-sensitive PKC by prolonged treatment with 4β-phorbol 12β-myristate 13α-acetate (PMA), the stimulatory effects of PGF 2α on glucose transport and GLUT1 mRNA accumulation were both inhibited. In accord, PMA was shown to stimulate GLUT1 mRNA accumulation. To further investigate if PKC may be activated by PGF 2α, we tested several diacylglycerol-sensitive PKC isozymes and found that PGF 2α was able to activate PKCε. Taken together, these results indicate that PGF 2α may enhance glucose transport in 3T3-L1 adipocytes by stimulating GLUT1 expression via a PKC-dependent mechanism.