Peptides released from bovine α-lactalbumin by simulated digestion alleviated free fatty acids-induced lipid accumulation in HepG2 cells

Abstract

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.

Keywords

• α-lactalbumin
• Peptide
• Lipid metabolism
• Molecular docking
• PPARα