Hypolipidemic effects and mechanisms of Val-Phe-Val-Arg-Asn in C57BL/6J mice and 3T3-L1 cell models

Abstract

Val-Phe-Val-Arg-Asn (VFVRN) has been identified and screened from lipid-lowering chickpea peptides (ChPs) previously. This work explored its lipid-lowering mechanisms by using a high-fat diet C57BL/6J mice model and 3T3-L1 preadipocyte cell model. Administration of VFVRN to hyperlipidemic mice significantly decreased the levels of total cholesterol (TC) and total triglyceride (TG) in liver and serum (P < 0.05), and increased the fecal triglyceride excretions. The expressions of sterol regulatory element-binding protein (SREBP)-2, liver X receptor (LXR)α, peroxisome proliferator-activated receptors (PPAR)α and their related target genes were regulated via AMP-activated protein kinase (p-AMPK) pathway in liver. Compared with model group, the levels of PPARα and PPARγ in 10 mg/kg VFVRN group were up-regulated by 36.96% and 36.49% in adipose tissues, while LXRα and ATP binding cassette G5/8 transporters (ABGC5/8) were lowered by 87.26% and 145% in small intestine respectively. Moreover, VFVRN promoted 3T3-L1 preadipocyte apoptosis by regulating the expressions of BaX, Caspase-3 and Bcl-2.

Keywords

• Val-Phe-Val-Arg-Asn (VFVRN)
• Hypolipidemic effects
• Transintestinal cholesterol efflux (TICE)
• 3T3-L1 preadipocyte
• Apoptosis