Abstract
Experiments have been conducted in which glucagon-induced stimulation of α-aminoisobutyric acid (AIB) transport in rat liver, presumably mediated by cyclic AMP, was markedly inhibited by actinomycin D, cycloheximide or puromycin. Inhibition of transport occurred despite the presence of high concentrations of cyclic AMP, suggesting that the nucleotide may act prior to, or at the same point as, the antibiotics. Kinetic studies showed that 1) the half-life of the glucagon-stimulated system(s) was less than 1 hour, and 2) glucagon treatment doubled V max without having any effect on the apparent K m for hepatic AIB transport. The results suggest that glucagon stimulates hepatic AIB transport by increasing the synthesis of some critical protein having a rapid turnover rate; this effect may be due to a prior increase in RNA synthesis.
Published Version
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