College of Food Science and Technology, Huazhong Agricultural University, Wuhan, China.
Key Laboratory of Environment Correlative Dietology (Huazhong Agricultural University), Ministry of Education, Wuhan, China.
J Sci Food Agric. 2019 Jan 30;99(2):576-586. doi: 10.1002/jsfa.9218. Epub 2018 Aug 6.
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.
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.
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.
绝经后女性缺乏雌激素是脂质代谢紊乱和肥胖的一个关键风险因素。除了使用雌激素替代疗法(ERT)的情况外,鹰嘴豆肽(ChP)可能是治疗高脂血症的潜在候选药物。
在去卵巢大鼠模型中,发现 ChP 可降低体重、脂肪组织大小、总胆固醇(TC)、总甘油三酯(TG)、低密度脂蛋白胆固醇(LDL-C)和血清及肝脏 TC 和 TG 的动脉粥样硬化指数(AI)。血清高密度脂蛋白胆固醇(HDL-C)、肝脏和粪便中的胆汁酸、粪便 TC 和 TG 显著增加(P<0.05)。ChP 可抑制脂肪酸合成酶(FAS)和 HMG-CoA 还原酶(HMGR)的活性。过氧化物酶体增殖物激活受体(PPAR)γ和固醇调节元件结合蛋白(SREBP)-1c 的表达下调,而 ChP 上调了肝 X 受体(LXR)α、雌激素受体(ER)α和 ERβ的表达。在 HepG2 细胞实验中,Mw<1 kDa 和 Mw<5 kDa ChP 级分处理后,细胞 TC 水平降低,NBD-胆固醇摄取量显著增加。Val-Phe-Val-Arg-Asn(VFVRN)可通过降低 HMGR 的表达来抑制胆固醇生物合成。
我们证明 ChP 可有效调节由雌激素缺乏引起的脂质代谢紊乱和肥胖。从 ChP 中鉴定出的 Val-Phe-Val-Arg-Asn 可降低 HMGR 的表达以抑制胆固醇生物合成。© 2018 化学工业协会。