1. Low intracellular concentrations of myo-inositol in diabetic cells may contribute to the development of tissue damage. The cause of these low levels is unknown, but inhibition of a putative myo-inositol transporter by high concentrations of glucose has been proposed. We have developed a triple-isotope method for estimating myo-inositol influx into human leucocytes and so investigated both the kinetics of this uptake in normal volunteers and the effect of glucose upon it.

2. Uptake was composed of a passive component with a rate constant of 2.4 ± 0.3 × 10−2 min−1 and a saturable component with a Km of 61 ± 23 μmol/l and a Vmax. of 11.3 ± 4.5 × 10−4 mmol min−1 l−1. Ouabain and low extracellular concentrations of sodium partly inhibited influx. Uptake was predominantly into the cytosolic fraction of the cell with 12% entering the membrane-associated fraction at both 5 and 10 min.

3. myo-inositol influx was significantly inhibited by both d- and l-glucose but not by sucrose. Neither cytochalasin B nor ethyl isopropyl amiloride significantly inhibited uptake.

4. It is concluded that a myo-inositol transporter exists in human leucocytes which is similar to that found in other species and tissues. Our technique allows myoinositol influx in diabetic subjects to be related to varying glycaemic control and tissue damage.

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