Effect of Amino Acid Deprivation on L-Alanine Uptake Through the Asc System in Freshly Isolated Trout Hepatocytes

Abstract

ABSTRACT Fasting in mammals and other vertebrates induces an increase in the ability of liver to extract from blood gluconeogenic substrates, such as plasma amino acids, which can also be used as an energy source (Cowey et al. 1977; Newsholme and Leech, 1983). In mammalian hepatocytes, food deprivation induces the appearance of a high-affinity component for short-chain amino acid transport, with the properties of system A, while there are no changes in the activities of a low-affinity system (the ASC system), system L (Fehlmann et al. 1979) or glutamine uptake (Hayes and McGivan, 1982). ‘A’ is the abbreviation for a Na+-dependent carrier which has L-alanine and other short-chain neutral amino acids as preferred substrates. Its tolerance to N-methylated analogues differentiates it from the ASC system. ‘L’ is the abbreviation for a Na+-independent carrier which has L-leucine as preferred substrate. ‘asc’ is the abbreviation for a carrier similar to the ‘ASC’ carrier with respect to preferred substrates, but it is Na+-independent. The ASC system is a widely distributed, short-chain neutral amino acid carrier that transports alanine, serine, cysteine and threonine in a Na+-dependent mode, although the scope of its substrates is now thought to be wider than when it was first described in Erlich ascites tumour cells (Christensen et al. 1967). Characteristically, it does not accept N-methylated amino acid derivatives (allowing easy distinction from the A system).