Neutral amino acids are transported by systems A, ASC, and L. In the previous companion study we demonstrated that 2-(methylamino) isobutyrate (
MeAIB) is a specific substrate for system A in muscle and that stimulation of system A by physiological concentrations of
insulin is preserved in acute
uremia (ARF).
Insulin-stimulated uptake of the nonspecific probes
cycloleucine and
alpha-aminoisobutyrate (AIB) is reportedly blunted by
uremia; the cause of this and whether transport by systems ASC and L is defective are unknown. In this study we examined these questions using incubated epitrochlearis muscles from normal fed, ARF, and
sham-operated control (SO) rats. System ASC was studied by measuring AIB and
cycloleucine uptake in the presence of inhibitors of systems A and L,
MeAIB and 2-amino-2-norbornane
carboxylic acid (BCH), respectively. System L was defined as
sodium-independent uptake suppressible by BCH. Excess
MeAIB completely inhibited
insulin-stimulated AIB and
cycloleucine uptake, indicating that system A is the only
insulin-responsive neutral
amino acid carrier in muscle. In ARF and SO mucles both AIB and
cycloleucine uptake were indistinguishable in the absence or presence of
insulin. Moreover, ARF caused no detectable abnormality in transport by systems ASC and L.