MYOINOSITOL IS AN OSMOLYTE IN RAT-LIVER MACROPHAGES (KUPFFER CELLS) BUT NOT IN RAW-264.7 MOUSE MACROPHAGES

The role of myo-inositol as an osmolyte was studied in cultured rat li ver macrophages (Kupffer cells). Hyperosmotic exposure of Kupffer cell s stimulated myo-inositol uptake and led to an increase in the mRNA le vels for the sodium/myo-inositol cotransporter (SMIT). Conversely, hyp o-osmotic (205 m-osM) exposure diminished myo-inositol uptake when com pared with normo-osmotic (305 m-osM) control incubations. The hyperosm olarity-induced SMIT mRNA increase was counteracted by added myo-inosi tol or betaine. In contrast with Kupffer cells, there was only a sligh t hyperosmotic stimulation of myo-inositol uptake in RAW 264.7 mouse m acrophages, and the myo-inositol transporter (SMIT) mRNA was not detec table. Further, a slight stimulation of taurine uptake and an increase in taurine transporter (TAUT) mRNA level by hyperosmolarity was obser ved in RAW 264.7 cells, whereas hypo-osmolarity led to a decrease in t aurine uptake and TAUT mRNA level. When Kupffer cells were preloaded w ith myo-inositol, hypo-osmotic exposure led to a rapid efflux of myo-i nositol from the cells. Myo-inositol efflux was also stimulated by pha gocytosis of latex particles; however, latex was without effect on the hyperosmolarity-induced increase of SMIT mRNA levels. The results sug gest a role of myo-inositol as an osmolyte in rat Kupffer cells but no t in RAW 264.7 mouse macrophages. The functional relevance of this osm olyte strategy might lie in the maintenance of cell volume homeostasis during phagocytosis in Kupffer cells; however, the interplay with the other osmolytes betaine and taurine remains to be established.