Transport and metabolic processes in the small intestine

Abstract

The transfer of a-methylglucoside and citrate was studied in experiments with everted sacs of rat and hamster small intestine. The transfer of α-methylglucoside was stimulated in the hamster by metabolizable hexoses and by citrate, succinate and pyruvate. In the rat jejunum only metabolizable hexoses were effective. Fluoride (10 mM) inhibited endogenous transfer in the hamster and glucose-dependent transfer in both rat and hamster. Fluoroacetate (10 mM) inhibited endogenous transfer in both animals, but inhibited glucose-dependent transfer only in the hamster. This indicated that in the hamster the citric acid cycle is the major source of energy both for endogenous substrate and for added glucose. In the rat, added glucose supplies energy mainly through the glycolytic pathway, although endogenous energy is derived from the citric acid cycle. In the rat, glucose abolished completely the inhibition of α-methylglucoside transfer produced by L-proline, although the inhibitory effects of galactose could only be partially overcome. In the hamster, L-proline caused an inhibition which was not completely abolished by the additional energy. The results indicate that in the rat sugars and amino acids compete for energy rather than interact at the carrier level. In the hamster it is possible that sugars and amino acids also interact at carrier level in addition to competing for energy. Citrate is more rapidly transferred and metabolized by hamster than by rat intestine. Citrate and unidentified radioactive metabolites accumulated in the serosal fluid, thus establishing the existence of a specific mechanism for citrate transfer.