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- W1954803374 abstract "ABSTRACT The mechanism of [3H]myo-inositol transport by the lobster hepatopancreas was examined using purified brush-border membrane vesicles. Transport was stimulated by a 100 mmol 1−1 inward Na+ gradient, but other cation gradients were ineffective, suggesting a Na+-dependent transfer mechanism. The transport system was most efficient at pH7·0 (both sides), rather than in the presence of a pH gradient (pHin = 7·0; pHout = 5·5) or at bilaterally low pH (pHin = pHout = 5·5). The system was shown to be electrogenic in two different ways. First, myo-inositol uptake was stimulated by anions of increasing permeability (SCN− > Cl− > gluconate). Second, an outwardly directed, valinomycin-induced K+ diffusion potential (inside negative) enhanced uptake in comparison with vesicles lacking the ionophore. Myo-inositol was transported by a carrier mechanism with an apparent Kt of 0·79mmoll−1, a Jmax of 6·3pmolmg protein−1 s−1, and by apparent diffusion with a permeability coefficient of 5·92 pmol mg protein−1s−1 (mmoll−1)−1. D-Glucose was a noncompetitive inhibitor of myo-inositol uptake, but myo-inositol did not significantly reduce the transport of D-[3H]glucose. Vesicles preloaded with myo-inositol trans-stimulated [3H]myo-inositol uptake, whereas those preloaded with D-glucose did not, suggesting that the inositol carrier did not transport D-glucose. It is proposed that myo-inositol does not share the glucose carrier, and that D-glucose may modulate inositol influx by binding to a ‘regulator’ site on the inositol carrier." @default.
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- W1954803374 date "1988-11-01" @default.
- W1954803374 modified "2023-10-15" @default.
- W1954803374 title "Inositol Transport by Hepatopancreatic Brush-Border Membrane Vesicles of the Lobster <i>Homarus Americanus</i>" @default.
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- W1954803374 doi "https://doi.org/10.1242/jeb.140.1.107" @default.
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