Corn-derived peptide LQQQLL alleviates skeletal muscle attenuation by mTOR signaling pathway and intestinal microbiota.

A novel peptide attenuating skeletal muscle atrophy was prepared, identified, screened from corn and its molecular mechanism was explored using two-step enzymatic hydrolysis, molecular docking, and sarcopenia mice model. The results showed that the DPPH free radical scavenging rate of corn peptides (CPs) was 45.20 % under the optimum preparation conditions. Fifty-one peptide fragments were identified from CPs, among which QQPIVGGA, QYQLPSY, LQQQLL, and LQQQQL presented superior affinity with mTORC1 and FOXO in molecular docking. LQQQLL (0.02 mM) significantly increased the proliferative activity of senescent C2C12 cells by 41.67 % compared with the model group (P < 0.05), showing the potential to attenuate skeletal muscle atrophy. The sarcopenia mice model results indicated that CPs and LQQQLL significantly improved the content of total superoxide dismutase (T-SOD), skeletal muscle mass index (SMI), and decreased the level of malondialdehyde (MDA), tumor necrosis factor (TNF)-α, muscle atrophy protein Fbox-1 (Atrogin-1), and 8-hydroxydeoxyguanosine (8-OHdG) (P < 0.05). CPs and LQQQLL also markedly increased the cross-sectional muscle area and the relative content of type II muscle fibers in sarcopenia mice. Additionally, CPs and LQQQLL significantly up-regulated the expression levels of PI3K, AKT and mTOR proteins (P < 0.05), reduced the proliferation of Proteobacteria, Actinobacteriota, Desulfobacterota, and Staphylococcus and promoted the proliferation of Bacteroidota, and Lactobacillus. In conclusion, CPs and LQQQLL could activate the PI3K/AKT/mTOR signaling pathway, and reduce the proliferation of pathogens and promote the proliferation of intestinal microorganisms, thus improving the attenuation of skeletal muscle.