Treatment with L-type amino acid transporter 1 inhibitor JPH203 enhances protein synthesis in C2C12 myotubes.

ABSTRACT: Excessive muscle protein synthesis causes skeletal muscle hypertrophy. Essential amino acids are substrates for muscle proteins and stimulate muscle protein synthesis. Several essential amino acids are taken up into muscle cells through L-type amino acid transporter 1 (LAT1). However, LAT1 may influence protein synthesis in an amino acid uptake-independent manner. Here, we investigated the effects of LAT1 inhibition on protein synthesis in C2C12 myotubes and the associated mechanisms. JPH203 (50 μM), a selective inhibitor of LAT1, stimulated protein synthesis without changing expression of phosphorylated p70S6K (T389) and 4EBP1 (T37/46), an indicator of mTORC1 activity. Culturing in amino acid-free media did not suppress JPH203-induced protein synthesis. The mTORC1 inhibitor rapamycin (100

SUBMITTER: Takegaki J 

PROVIDER: S-EPMC12630651 | biostudies-literature | 2025 Nov

REPOSITORIES: biostudies-literature