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Synergistic effect of prostaglandin F2α and cyclic AMP on glucose transport in 3T3‐L1 adipocytes
Author(s) -
Chiou GuangYuh,
Fong Jim C.
Publication year - 2004
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.20338
Subject(s) - cycloheximide , protein kinase c , glut1 , glucose transporter , medicine , activator (genetics) , endocrinology , prostaglandin f2alpha , chemistry , 3t3 l1 , phorbol , glucose uptake , prostaglandin , diacylglycerol kinase , northern blot , protein kinase a , adipocyte , insulin , biology , biochemistry , phosphorylation , messenger rna , adipose tissue , protein biosynthesis , receptor , gene
The combined effect of prostaglandin F2α (PGF2α) and cAMP on glucose transport in 3T3‐L1 adipocytes was examined. In cells pretreated with PGF2α and 8‐bromo cAMP for 8 h, a synergy between these two agents on glucose uptake was found. Insulin‐stimulated glucose transport, on the other hand, was only slightly affected. The synergistic effect of these two agents was suppressed in the presence of cycloheximide and actinomycin D. In concord, immunoblot and Northern blot analyses revealed that GLUT1 protein and mRNA levels were both increased in cells pretreated with both PGF2α and 8‐bromo cAMP, greater than the additive effect of each agent alone. The synergistic action of PGF2α with 8‐bromo cAMP to enhance glucose transport 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, a PKC activator, the synergistic effects of PGF2α and 8‐bromo cAMP on glucose transport and GLUT1 mRNA accumulation were both abolished. Taken together, these results indicate that PGF2α may act with cAMP in a synergistic way to increase glucose transport, probably through enhanced GLUT1 expression by a PKC‐dependent mechanism. © 2004 Wiley‐Liss, Inc.