Prostaglandin F2α increases glucose transport in 3T3-L1 adipocytes through enhanced GLUT1 expression by a protein kinase C-dependent pathway

The effect of prostaglandin F-2alpha (PGF(2alpha)) on glucose transport in differentiated 3T3-L1 adipocytes was examined. Whereas PGF(2alpha) 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(2alpha) 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(2alpha). The effect of PGF(2alpha) 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 4beta-phorbol 12beta-myristate 13alpha-acetate (PMA), the stimulatory effects of PGF(2alpha). 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(2alpha), we tested several diacylglycerol-sensitive PKC isozymes and found that PGF(2alpha) was able to activate PKCepsilon. Taken together, these results indicate that PGF(2alpha) may enhance glucose transport in 3T3-L1 adipocytes by stimulating GLUT] expression via a PKC-dependent mechanism. (C) 2003 Elsevier Inc. All rights reserved.