Concentration of myo-inositol in skeletal muscle of the rat occurs without active transport.

The cellular uptake of nonphosphorylated myo-inositol (MI) and its incorporation into phosphoinositide in the rat epitrochlearis muscle was measured. Cellular uptake of [2-(3)H]MI was determined by the difference between total uptake and [2-(3)H]MI present in the extracellular fluid determined with [1-(14)C]mannitol. Cellular uptake was parabolic and directly proportional to medium MI concentrations between 25 and 3,200 muM. Saturation of a MI carrier was not evident. Moreover, uptake was not inhibited by 2 mM ouabain, 0.3 mM 2,4-dinitrophenol, or 22 mM glucose. Insulin, 100 mU/ml, was without effect on either cellular uptake of [2-(3)H]MI or its incorporation into phosphoinositides. In muscles that were preloaded with [2-(3)H]MI and then incubated in media that contained a constant amount of MI but no [2-(3)H]MI, 44.3% of the [2-(3)H]MI was released after 10 min increasing to 62.5% by 120 min. Cellular MI concentrations were 0.18 mumol/g wet tissue (four times plasma levels) in rapidly isolated and frozen epitrochlearis muscle. When muscle was incubated without MI, 48% of endogenous MI was lost rapidly. Restoration of cellular MI in 50 muM MI media occurred in two phases, a rapid uptake phase lasting 10 min and a subsequent slow phase of MI uptake. It is concluded that MI enters and leaves skeletal muscle cells freely by a process that does not involve active transport. Neither insulin nor hyperglycemia affected MI transport nor its incorporation into phosphoinositides. The intracellular to medium concentration gradient may be dependent on reversible binding to tubulin and possibly to other intracellular components.