Abstract
Estimations of steady-state fluxes of divalent Fe across rat intestinal segments in vitro provide evidence for two active transport mechanisms. Segments of the distal small intestine transport the mineral against electrochemical potential gradients from the serosal to the mucosal surface. Active transport in the reverse direction was confirmed with segments of proximal duodenum. The distal mechanism is dependent on cellular metabolism and is markedly decreased by metabolic inhibitors or in the absence of a metabolizable hexose. Cycloheximide, which inhibits protein biosynthesis, also blocks the active transport. Perfusion of jejunal and duodenal intestinal loops in situ in anesthetized rats provides evidence that endogenous Fe can be transferred to the lumen by a process otherthan shedding of mucosal cells. It is suggested that such transfer may occur via the active transport mechanism.

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