title: Prostaglandin F2alpha increases glucose transport in 3T3-L1 adipocytes through enhanced GLUT1 expression by a protein kinase C-dependent pathway.
abstract: The effect of prostaglandin F2alpha (PGF2alpha) on glucose transport in differentiated 3T3-L1 adipocytes was examined. Whereas PGF2alpha 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 PGF2alpha 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 PGF2alpha. The effect of PGF2alpha 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 PGF2alpha 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 PGF2alpha, we tested several diacylglycerol-sensitive PKC isozymes and found that PGF2alpha was able to activate PKCepsilon. Taken together, these results indicate that PGF2alpha may enhance glucose transport in 3T3-L1 adipocytes by stimulating GLUT1 expression via a PKC-dependent mechanism.
authors.affiliation: Institute of Biochemistry, National Yang-Ming University, Taipei 112 , Taiwan, ROC. ffong@ym.edu.tw
authors.forename: Guang Yuh
authors.initials: GY
authors.lastname: Chiou
authors.forename: Jim C
authors.initials: JC
authors.lastname: Fong
mesh_terms: D041721:3T3-L1 Cells; D000818:Animals; D001692:Biological Transport; D003513:Cycloheximide / Q000494:pharmacology; D004268:DNA-Binding Proteins; D003609:Dactinomycin / Q000494:pharmacology; D003847:Deoxyglucose / Q000378:metabolism; D015237:Dinoprost / Q000494:pharmacology*; D004791:Enzyme Inhibitors / Q000494:pharmacology; D005947:Glucose / Q000378:metabolism*; D051272:Glucose Transporter Type 1; D007211:Indoles / Q000494:pharmacology; D008301:Maleimides / Q000494:pharmacology; D051379:Mice; D009004:Monosaccharide Transport Proteins / Q000378:metabolism*; D010703:Phorbol Esters / Q000494:pharmacology; D011493:Protein Kinase C / Q000037:antagonists & inhibitors / Q000378:metabolism*; D051744:Protein Kinase C-epsilon; D012333:RNA, Messenger / Q000378:metabolism; D015398:Signal Transduction / Q000187:drug effects; D014157:Transcription Factors / Q000378:metabolism*
chemical_list: D004268:DNA-Binding Proteins; D004791:Enzyme Inhibitors; D051272:Glucose Transporter Type 1; D007211:Indoles; D008301:Maleimides; D009004:Monosaccharide Transport Proteins; D010703:Phorbol Esters; D012333:RNA, Messenger; C480633:SLC2A4RG protein, human; C495678:Slc2a1 protein, mouse; D014157:Transcription Factors; D003609:Dactinomycin; D003513:Cycloheximide; D003847:Deoxyglucose; D015237:Dinoprost; C497256:Prkce protein, mouse; D011493:Protein Kinase C; D051744:Protein Kinase C-epsilon; D005947:Glucose; C070515:bisindolylmaleimide I