Enhanced small neutral but not branched chain amino acid transport after epigenetic sodium coupled neutral amino acid transporter‐2 (SNAT2) cDNA expression in myoblasts

Background Skeletal muscle mass and function are partly maintained by the supply of amino acids, altered acid transport is an important cause frailty that can lead to decreased independence with increasing age slow trauma recovery. The system-A sodium coupled neutral transporter (SNAT)-2 coded gene family SLC38A2 generates a 506 56 kDa protein acids in skeletal muscle. Ageing associated decrease expression SNAT2 transporters. Methods In this study, we used C2C12 cell line, using myoblast cells differentiated into myotubes. We investigated if DNA would enhance intracellular levels increase their availability for synthesis. Results control myoblasts myotubes, found significantly (6.5× decrease, n = 4 per group, P < 0.05) myotubes than myoblasts. After transfection SNAT2-eGFP cDNA plasmid, increased perinuclear punctate persisted was more cytoplasmic after differentiation Interestingly, transfected were responsive hormone 5α-dihydrotestosterone (DHT, 4.5 nM, 1.6×, 3 0.04). Starvation enhanced C14-MeAIB (1.7×, indicating SNAT2. Inhibiting high concentrations MeAIB (3.3 or 5 mM) reduced C14-Isoleucine L-type (LAT2, 52.8% 77%, respectively, 0.05). However, there no LAT2 C14-isoleucine detectable DHT (4.5 nM) exposure. This indicated small not rate limiting Conclusions Overall, these data show its following starvation treatment physiological DHT. Enhanced offers viable epigenetic target pathological conditions transport.