Background: The lack of estrogen in postmenopausal women is a key risk factor for disorders of lipid metabolism and for obesity. Except in cases where estrogen replacement therapy (ERT) is being used, chickpea peptides (ChPs) may be a potential candidate for treating hyperlipidemia.
Results: In ovariectomized rats model, ChPs were found to decrease body weight, adipose tissue size, total cholesterol (TC), total triglyceride (TG), low-density lipoprotein cholesterol (LDL-C), and the atherogenic index (AI) in serum and liver TC and TG. Serum high-density lipoprotein cholesterol (HDL-C), bile acids in liver and feces, fecal TC and TG were observed to increase significantly (P < 0.05). ChPs play a role in inhibiting the activities of fatty acid synthetase (FAS) and HMG-CoA reductase (HMGR). The expression of peroxisome proliferator-activated receptors (PPAR)γ and sterol regulatory element-binding protein (SREBP)-1c were downregulated and the expression of liver X receptor (LXR) α, estrogen receptor(ER)α and ERβ were upregulated by ChPs. In HepG2 cell experiments, the cellular TC levels decreased and the uptake of NBD-cholesterol increased significantly after treatment with Mw < 1 kDa and Mw < 5 kDa ChPs fractions. Val-Phe-Val-Arg-Asn (VFVRN) could inhibit TC biosynthesis by decreasing the expression of HMGR.
Conclusion: We demonstrated that ChPs could effectively regulate lipid metabolism disorders and restrain obesity caused by estrogen deficiency. Val-Phe-Val-Arg-Asn identified from ChPs could reduce the expression of HMGR to inhibit cholesterol biosynthesis. © 2018 Society of Chemical Industry.
Keywords: Chickpea peptides (ChPs); Val-Phe-Val-Arg-Asn; estrogen receptor; hypolipidemic effects; ovariectomized rats.
© 2018 Society of Chemical Industry.