Angiotensin-converting enzyme inhibitory peptide IVGFPAYGH protects against liver injury in mice fed a high‑sodium diet by inhibiting the RAS and remodeling gut microbial communities

Abstract

Consuming a high‑sodium diet carries serious health risks and significantly influences the activation state of the renin-angiotensin system (RAS). This study evaluates the protective effect of angiotensin-converting enzyme (ACE) inhibitory peptide IVGFPAYGH on a high‑sodium diet–induced liver injury. IVGFPAYGH supplementation increased the activities of liver antioxidase and decreased the levels of liver inflammatory factor in mice fed a high‑sodium diet (8 % NaCl). IVGFPAYGH supplementation also reduced liver fatty acid synthesis and promoted fatty acid oxidation, increased the expression of low-density lipoprotein receptor, and improved liver dyslipidemia. Furthermore, IVGFPAYGH supplementation inhibited the activation of the liver RAS via inhibiting ACE activity and reducing angiotensin II levels in mice fed a high‑sodium diet. Moreover, IVGFPAYGH supplementation could alter the gut microbiota composition toward a normal gut microbiota composition and increase the abundance of the Lactobacillus genus. IVGFPAYGH supplementation also increased the expression levels of small intestinal tight junction protein and cecum short-chain fatty acids. Thus, IVGFPAYGH supplementation may maintain intestinal homeostasis and improve high‑sodium diet–induced liver injury by altering the gut microbiota composition and inhibiting the RAS. IVGFPAYGH is a promising functional ingredient for protecting liver damage caused by a high‑sodium diet.