Lee Kyu-Shik, Chun So-Young, Kwon Yun-Suk, Kim Soyoung, Nam Kyung-Soo
Department of Pharmacology and Intractable Disease Research Center, School of Medicine, Dongguk University, Gyeongju, Gyeongsangbuk‑do 38066, Republic of Korea.
Mol Med Rep. 2017 May;15(5):2814-2822. doi: 10.3892/mmr.2017.6317. Epub 2017 Mar 13.
A high‑fat diet or high‑cholesterol diet (HCD) is a major cause of metabolic diseases, including obesity and diabetes; vascular diseases, including hypertension, stroke and arteriosclerosis; and liver diseases, including hepatic steatosis and cirrhosis. The present study aimed to evaluate the effects of deep sea water (DSW) on rats fed a HCD. DSW decreased HCD‑induced increases in total cholesterol and low‑density lipoprotein (LDL) cholesterol in the blood, and recovered high‑density lipoprotein cholesterol. In addition, DSW decreased levels of liver injury markers, which were increased in response to HCD, including glutamate‑oxaloacetate transaminase, glutamate‑pyruvate transferase and alkaline phosphatase. Lower lipid droplet levels were observed in the livers of rats fed a HCD and treated with DSW at a hardness of 1,500, as compared with those in the HCD only group. Semi‑quantitative reverse transcription‑polymerase chain reaction (RT‑PCR) revealed that mRNA expression levels of fatty acid synthase and sterol regulatory element binding protein‑1c (SREBP‑1c) in rats fed a HCD with DSW were lower compared with the HCD only group. Furthermore, quantitative RT‑PCR revealed that DSW enhanced LDL receptor (LDLR) mRNA expression in a hardness‑dependent manner. Combined, the results of the present study indicated that DSW may reduce HCD‑induced increases in blood and liver lipid levels, indicating that DSW may protect against hypercholesterolemia and non‑alcoholic hepatic steatosis. In addition, the present study demonstrated that DSW‑induced downregulation of lipids in the blood and hepatic lipid accumulation was mediated by enhancement of LDLR expression and suppression of fatty acid synthase and SREBP‑1c.
高脂饮食或高胆固醇饮食(HCD)是包括肥胖症和糖尿病在内的代谢性疾病、包括高血压、中风和动脉硬化在内的血管疾病以及包括肝脂肪变性和肝硬化在内的肝脏疾病的主要病因。本研究旨在评估深海海水(DSW)对喂食HCD的大鼠的影响。DSW降低了HCD诱导的血液中总胆固醇和低密度脂蛋白(LDL)胆固醇的升高,并使高密度脂蛋白胆固醇恢复正常。此外,DSW降低了肝脏损伤标志物的水平,这些标志物在HCD作用下升高,包括谷草转氨酶、谷丙转氨酶和碱性磷酸酶。与仅喂食HCD的组相比,在喂食HCD并接受硬度为1500的DSW处理的大鼠肝脏中观察到更低的脂滴水平。半定量逆转录-聚合酶链反应(RT-PCR)显示,与仅喂食HCD的组相比,喂食HCD并补充DSW的大鼠中脂肪酸合酶和固醇调节元件结合蛋白-1c(SREBP-1c)的mRNA表达水平更低。此外,定量RT-PCR显示,DSW以硬度依赖的方式增强低密度脂蛋白受体(LDLR)的mRNA表达。综合来看,本研究结果表明,DSW可能降低HCD诱导的血液和肝脏脂质水平升高,表明DSW可能预防高胆固醇血症和非酒精性肝脂肪变性。此外,本研究表明,DSW诱导的血液脂质下调和肝脏脂质积累是通过增强LDLR表达以及抑制脂肪酸合酶和SREBP-1c介导的。