A submucosal mechanism of action for prostaglandin E2 on hexose absorption and metabolism in mouse intestine.

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1. The involvement of prostaglandin E2 (PGE2) in hexose absorption and metabolism was studied in mouse small intestinal villus cells. 2. Phlorizin-sensitive, Na(+)-dependent alpha-methyl-D-glucoside (alpha-MG) uptake (0.8 mM) during 2 min cell incubations (37 degrees C) was 74 +/- 4 nmol (mg protein)-1. Maximal uptake was 110 +/- 8 nmol (mg protein)-1, representing an accumulation of 50-fold. Metabolism of D-glucose (5 mM) to L-lactate was 38 nmol min-1 (mg protein)-1. 3. Incubation of isolated cells with indomethacin or PGE2 did not affect alpha-MG uptake or D-glucose metabolism. By including indomethacin during cell isolation from whole intestine, alpha-MG uptake was inhibited dose dependently (50-250 microM) by up to 70% (P < 0.001). PGE2 present during both isolation and incubation inhibited by 85% (P < 0.001) at 1 microM and by 27% (P < 0.05) at 0.1 microM, with no effect at lower concentrations. alpha-MG uptake was reduced to 38% (P < 0.01) when 1 microM-PGE2 and 250 microM-indomethacin were presented in combination. When present during cell isolation and incubation, 1 microM-PGE2 inhibited lactate production by 24% (P < 0.05), except when present in combination with 250 microM-indomethacin. Indomethacin, itself, had no effect on lactate production. 4. A submucosal mechanism is proposed to account for the observed inhibitory effects of PGE2 on brush-border uptake of alpha-MG and cellular lactate production. Indomethacin appears to exert not only an effect of its own, possibly via PG-independent actions within the submucosa, but at high concentrations also disrupts the effects of exogenously applied PGE2.

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