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富含多糖的红藻(角叉菜)热水提取物可改善高脂饮食喂养大鼠的血浆胆固醇和肝脂稳态的改变。

Polysaccharide-rich red algae (Gelidium amansii) hot-water extracts ameliorate the altered plasma cholesterol and hepatic lipid homeostasis in high-fat diet-fed rats.

机构信息

Graduate Institute of Toxicology, College of Medicine, National Taiwan University, Taipei 10051, Taiwan.

Department of Medical Research, China Medical University Hospital, China Medical University, Taichung 40402, Taiwan.

出版信息

J Food Drug Anal. 2021 Mar 15;29(1):46-56. doi: 10.38212/2224-6614.1181.

Abstract

We have demonstrated that red algae Gelidium amansii (GA) hot-water extract (GHE) is a polysaccharide-rich fraction, containing 68.54% water-soluble indigestible carbohydrate polymers; the molecular weight of major polysaccharide is 892. Here, we investigated the mechanisms of GHE on plasma and hepatic lipid metabolisms in high-fat (HF) diet-fed rats. Rats were divided into: normal diet group, HF-diet group, HF-diet+5% GHE group, and HF-diet+1% cholestyramine group. GHE supplementation for 8 weeks significantly decreased plasma cholesterol, LDL-C, and VLDL-C levels and increased the fecal triglyceride and bile acid excretion in HF diet-fed rats. GHE group has lower lipid contents in the liver and adipose tissues. GHE supplementation decreased the activities of acetyl-CoA carboxylase, fatty acid synthase, and HMG-CoA reductase in the livers. The levels of increased phosphorylated AMP-activated protein kinase (AMPK), peroxisome proliferator activated receptor (PPAR)-α, farnesoid-X receptor (FXR), low density lipoprotein receptor (LDLR), and cytochrome P450-7A1 (CYP7A1) protein expression, and the decreased PPAR-γ protein expression in the livers were observed in GHE group. These results suggest that GHE supplementation is capable of interfering in cholesterol metabolism and increasing hepatic LDLR and CYP7A1 expression to decrease blood cholesterol, and activating FXR and AMPK to inhibit lipogenic enzyme activities and reduce the hepatic lipid accumulation.

摘要

我们已经证明,红藻石花菜(GA)热水提取物(GHE)是一种富含多糖的部分,含有 68.54%的水溶性不可消化的碳水化合物聚合物;主要多糖的分子量为 892。在这里,我们研究了 GHE 对高脂肪(HF)饮食喂养大鼠的血浆和肝脂质代谢的机制。大鼠分为:正常饮食组、HF 饮食组、HF 饮食+5%GHE 组和 HF 饮食+1%考来烯胺组。8 周的 GHE 补充显著降低了 HF 饮食喂养大鼠的血浆胆固醇、LDL-C 和 VLDL-C 水平,并增加了粪便甘油三酯和胆汁酸排泄。GHE 组肝脏和脂肪组织中的脂质含量较低。GHE 补充降低了肝脏中乙酰辅酶 A 羧化酶、脂肪酸合成酶和 HMG-CoA 还原酶的活性。在 GHE 组中观察到磷酸化 AMP 激活蛋白激酶(AMPK)、过氧化物酶体增殖物激活受体(PPAR)-α、法尼醇 X 受体(FXR)、低密度脂蛋白受体(LDLR)和细胞色素 P450-7A1(CYP7A1)蛋白表达增加,以及 PPAR-γ 蛋白表达降低。这些结果表明,GHE 补充能够干扰胆固醇代谢,增加肝脏 LDLR 和 CYP7A1 的表达,降低血液胆固醇,并激活 FXR 和 AMPK,抑制脂肪生成酶的活性,减少肝脏脂质堆积。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6a82/9261851/dfa6301a7c40/jfda-29-01-046f1.jpg

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