Prostaglandin F(2)alpha 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 l evels of glucose transporter (GLUT) 1 protein in 3T3-L1 adipocytes. Since A A is a precursor of prostaglandins (PGs), we investigated the effect of PGs on glucose consumption in 3T3-L1 cells. Among several PGs, only prostaglan din F(2)alpha (PGF(2)alpha) enhanced glucose consumption in 3T3-L1 cells tr eated with dexamethasone (DEX), 3-isobutyl-1-methyl-xanthine (IBMX), and in sulin. To study the mechanism of PGF(2)alpha-enhanced glucose consumption, we investigated the effect of PGF(2)alpha on glycerol-3-phosphate dehydroge nase (GPDH) activity, triglycerides (TGs) content, and the expression of GL UT1 protein. PGF(2)alpha suppressed GPDH activity and did not increase the expression of GLUT1 protein in 3T3-L1 cells treated with DEX, IBMX, and ins ulin. These results suggest that PLA-stimulated glucose uptake is not throu gh the effect of PGF(2)alpha. Our results indicate that PGF(2)alpha is a un ique regulator of adipocyte differentiation (suppression) and glucose consu mption (enhancement) in 3T3-L1 cells. (C) 2001 Elsevier Science Inc. All ri ghts reserved.