Deep sea water improves hypercholesterolemia and hepatic lipid accumulation through the regulation of hepatic lipid metabolic gene expression

Abstract

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.