Aim: Properly controlled nutrition is an important factor for the successful outcome of dental implant treatments. Following digestion, excess amino acids absorbed from the intestine are stored in skeletal muscle. During starvation, this reservoir of amino acid can be released from skeletal muscle into the blood supply. In skeletal muscle tissue, Tas1r1/Tas1r3 has been shown to repress autophagy, and regulate amino acids metabolism. However, the exact mechanism by which Tas1r1/Tas1r3 regulates the storage and release of amino acids remains to be elucidated. Here, we report that the expression levels of Tas1r1 and Tas1r3 are decreased upon serum starvation of muscle fibers in vitro.
Materials and Methods: C2C12 cells were cultured and maintained in DMEM supplemented with 10% fetal bovine serum in 5% CO2. Single fibers of skeletal muscle and associated satellite cells were prepared from the extensor digitorum longus muscle of 8-week-old C57BL/6 mouse. To compare Tas1r1, Tas1r3, and Autophagy related genes expression in starved C2C12 cells, the datasets GSE925 were downloaded from the PubMed GEO and analysed.
Results: Tas1r1 and Tas1r3 was expressed by activated satellite cells, skeletal muscle stem cells and muscle fibers in vitro. The expression levels of Tas1r1/Tas1r3 in primary satellite cells increased with their differentiation. In silico and quantitative PCR analysis revealed that the expression levels of both Tas1r1 and Tas1r3 are decreased in serum-starved C2C12 cells.
Conclusion: Our data suggests that the reduction of Tas1r1/Tas1r3 induces autophagy and contributes to the release of amino acids into the blood stream from skeletal muscle tissue.