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

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.