To elucidate how intracellular L-alanine enhances water transport across the seawater eel intestine, effects of various metabolic inhibitors were examined. The L-alanine-induced water flux was inhibited by amino-oxyacetate, an inhibitor of aminotransferase. After blocking the synthesis of pyruvate from L-alanine with this drug, water transport was stimulated with pyruvate, whose effects were inhibited by oxythiamine, an inhibitor of pyruvate dehydrogenase. 2,4-Dinitrophenol (DNP) also inhibited the effects of L-alanine. Furthermore, L-alanine enhanced ouabain-sensitive O2 consumption in this tissue, and the enhancement in O2 consumption preceded that in the transepithelial potential difference (PD) and the net water flux. These results indicate that L-alanine is metabolized through the citric acid cycle to produce ATP, and that a metabolic product stimulates ion and water transport. L-Glutamine also seems to be metabolized just like L-alanine because: L-glutamine acted from inside the enterocyte; DNP inhibited the effects of L-glutamine; neither of the effects of L-glutamine and L-alanine were additive but they were mutually complementary; L-glutamine also enhanced ouabainsensitive O2 consumption; and the increment in O2 consumption preceded that in the PD and the net water flux. The effects of L-glutamine on the PD and the net water flux depended on glutamine concentration and the concentration-response curve was of the Michaelis-Menten type, indicating that the rate of L-glutamine uptake into the enterocyte limits the overall rate of L-glutamine metabolism. A regulatory role of amino acids for ion and water transport is discussed.

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