Inter-organ nitrogen exchange during prolonged starvation in the rat
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abstract
During starvation, enhanced nitrogen loss occurs from various organs. Glutamine and alanine have been suggested to be the main nitrogen carriers from peripheral to splanchnic tissues. In the liver, these amino acids are precursors for urea synthesis and thus can provide substrates for gluconeogenesis. To study inter-organ nitrogen transport during prolonged starvation, glutamine, alanine, ammonia and urea exchange was measured across the hindquarter, the portal drained viscera and the liver in male Wistar rats in the fed state or fater 1, 2, 3, or 4 days of fasting. Arterial urea increased in time (p < 0.05), but glutamine, alanine and ammonia did not change. Hindquarter glutamine and alanine release increased and reached a maximum at day 3, after which it declined. Simultaneously, portal drained viscera glutamine uptake, as well as alanine and ammonia release decreased at day 3 of starvation, while liver glutamine release switched to uptake at day 2 of starvation, coinciding with maximal urea release. In the course of starvation, an increasing proportion of hepatic urea release could be accounted for by hepatic uptake of blood derived glutamine, alanine and ammonia. These results demonstrate that during prolonged starvation in the rat important differences exist in the pattern of glutamine and alanine exchange across muscle, gut and liver. The different time course of hepatic urea release and muscle glutamine and alanine release suggests that, besides muscle, other organs also are important in total body nitrogen loss during prolonged starvation in the rat.
