Abstract
• Peptides from α-LA decreased lipid accumulation in HepG2 cells. • The peptides of P2 (GINY) and P8 (DQW) acted as PPARα ligands. • P2 and P8 up-regulated genes expression of fatty acid β-oxidation in HepG2 cells. • P2 and P8 down-regulated genes expression of lipogenesis in HepG2 cells. Our previous study showed that α-lactalbumin (α-LA) has a regulatory effect on lipid metabolism in obese mice. In this study, we performed simulated gastrointestinal digestion of α-LA to investigate the effect of peptides on lipid metabolism in HepG2 cells. The results showed that α-LA hydrolysate attenuated lipid accumulation and enhanced PPARα levels in HepG2 cells. Then, peptides from the hydrolysate were isolated and purified, and four PPARα-activating peptides (P2 (GINY), P8 (DQW), P13 (DQWL), P14 (LFQ)) were screened by molecular docking. Interestingly, P2 and P8 effectively improved intracellular TG and PPARα levels than P13 and P14. Furthermore, P2 and P8 acted as PPARα ligands to activate the PPARα signalling pathway, upregulate the expression of β-oxidation-related genes (PPARα, CPT-1a, ACOX1) and downregulate the expression of lipogenesis-related genes (ACC1, SCD-1, FASN), thereby improving lipid metabolism and reducing oxidative stress damage. Hence, α-LA shows promise as a functional food to ameliorate obesity.
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