Kinetics of glucose transport by the perfused mid‐gut of the freshwater prawn Macrobrachium rosenberg ii.

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Abstract
Mucosal influx of [3H]glucose was examined in the mid-gut of a freshwater prawn, M. rosenbergii, using an in vitro perfusion technique. [3H]glucose transfer across the apical cell membrane of the epithelium exhibited Michaelis-Menten kinetics .**GRAPHIC**. = 0.15 .mu.mole glucose equiv/g.cntdot.min, Kt = 0.17 mM). Under Na-free conditions, glucose influx was significantly reduced and a linear function of substrate concentration, indicative of either slow cellular diffusion (KK= 7.6 .times. 10-3 .mu.mole glucose equiv/g.cntdot.min.cntdot.mM) or a facilitated process with a low carrier affinity for the sugar. Phlorizin was a potent competitive inhibitor of glucose influx (Ki = 3.6 .times. 10-3 mM), galactose and 3-O-methylglucose (3-O-MG) were weak inhibitors, and fructose had no evident effect on glucose uptake. Azide, but not iodoacetate (IAA), significantly depressed influx. Absorbed [3H]glucose was rapidly metabolized by the mid-gut. The majority of accumulated activity within the tissue was in the form of phosphorylated compounds and tritiated water (THO), while only 0-3% was recovered as free-glucose. Preliminary studies examining transmural [3H]glucose transport, demonstrated a significant net mucosal to serosal free-glucose flux across the prawn mid-gut which was Na-dependent and IAA- and phlorizin-sensitive. Two alternative interpretations of the data are advanced as possible mechanisms for transepithelial glucose transport: group translocation, or the operation of an energized, high affinity, baso-lateral sugar transport carrier.

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