Low-Dose Fish Oil Consumption Prevents Hepatic Lipid Accumulation in High Cholesterol Diet Fed Mice

Department of Clinical Dietetics and Human Nutrition, Josai University, Faculty of Pharmaceutical Sciences, Keyakidai 1-1, Sakado, Saitama 350-0295, Japan.
Journal of Agricultural and Food Chemistry (Impact Factor: 3.11). 11/2011; 59(24):13353-9. DOI: 10.1021/jf203761t
Source: PubMed

ABSTRACT We examined the effects of low-dose fish oil ingestion on hepatic lipid accumulation caused after high cholesterol feeding in C57BL/6J mice. The mice were fed purified experimental diets consisting of 20 energy % (en%) safflower oil (SO or SO/CH), 2 en% fish oil + 18 en% safflower oil (2FO or 2FO/CH), or 5 en% fish oil + 15 en% safflower oil (5FO or 5FO/CH) with or without 2 weight % (wt %) cholesterol for 8 weeks. Hepatic triglyceride and total cholesterol contents were significantly lower in groups that were fed diets containing fish oil and cholesterol than in those that were fed safflower oil and cholesterol. The hepatic mRNA levels of fatty acid synthase (FAS) were lower in groups fed cholesterol or fish oil. Fatty acid oxidation-related hepatic gene expressions were higher in fish oil-fed groups. Fecal cholesterol excretion was higher in all cholesterol-fed groups; cholesterol excretion was high in groups fed fish oil and cholesterol. These results suggest that low-dose fish oil diets improve lipid metabolism by modifying the expression of lipid metabolism-related genes in the liver and increasing fecal cholesterol excretion.

  • [Show abstract] [Hide abstract]
    ABSTRACT: Non-alcoholic fatty liver disease (NAFLD) is defined as excess of fat in the liver. We investigated the effects of black soybean on the cholesterol metabolism and insulin resistance of mice fed high cholesterol/fat diets. Mice were randomly allocated into 4 groups that were fed different diets: the normal cholesterol/fat diet; high cholesterol/fat diets (HCD); and HCD with 1%, and 4% black soybean powder (1B-HCD, and 4B-HCD). Liver total cholesterol and triglyceride concentrations were significantly lower in the black soybean-supplemented groups than that in the HCD group. PCR revealed significantly lower hepatic SREBP2 and HMG-CoA reductase mRNA levels of black soybeansupplemented mice. Real-time PCR revealed significantly higher hepatic ABCA1 mRNA level of black soybean-supplemented mice, which may increase cholesterol efflux. Liver bile acids concentration was significantly high in the 4B-HCD group. Black soybean stimulated secretion of adiponectin, activation of pAMPK, and eliminated free fatty acids in the liver. Black soybean supplementation decreased MDA and nitrate level. The activities of SOD, catalase, and GPx were restored by black soybean supplementation. Our data strongly indicate that black soybean influences the balance between oxidative and antioxidative stress. We suggest that black soybean improves cholesterol metabolism, insulin resistance, and alleviates oxidative damage in NAFLD.
    Food and chemical toxicology: an international journal published for the British Industrial Biological Research Association 07/2013; DOI:10.1016/j.fct.2013.07.048 · 2.99 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: The potential mechanism of the hypocholesterolemic effect of capsaicinoids in rats fed with cholesterol-enriched and cholesterol-free diets was determined. Capsaicinoids favorably modified the lipoprotein profile of rats. Capsaicinoids consumption down-regulated the mRNA levels of hepatic 3-hydroxyl-3-methylglutaryl CoA (HMG-CoA) reductase by 0.55-fold and hepatic cholesterol-7α-hydroxylase (CYP7A1) by 0.53-fold in the cholesterol-free diet group (P < 0.05) but up-regulated the CYP7A1 level by 1.38-fold in the cholesterol-enriched diet group (P < 0.05). It also increased the expression levels of ileal bile acid binding protein and apical sodium-dependent bile acid transporter in the ileum, as well as transient receptor potential vanilloid type-1 in the liver and ileum in the different groups. Capsaicinoids reduced the amount of bile acids in feces by -15.97% and contents of the small intestine by -9.64% in the cholesterol-free diet group (P < 0.05) but increased both by 13.06% and 10.20%, respectively, in the cholesterol-enriched diet group. The cholesterol-lowering action of capsaicinoids in the cholesterol-free diet group was attributed to the inhibition of hepatic cholesterol synthesis, whereas that in the cholesterol-enriched diet group was attributed to the stimulation of the conversion of cholesterol to bile acids and the increasing excretions of bile acids in feces.
    Journal of Agricultural and Food Chemistry 04/2013; 61(18). DOI:10.1021/jf304471t · 3.11 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: The aim of the current study is to examine the improving effect of Sasa borealis stem (SBS) extract extracts on high-fat diet (HFD)-induced hepatic steatosis in rats. To determine the hepatoprotective effect of SBS, we fed rats a normal regular diet (ND), HFD, and HFD supplemented with 150 mg/kg body weight (BW) SBS extracts for five weeks. We found that the body weight and liver weight of rats in the HFD + SBS group were significantly lower than those in the HFD group. Significantly lower serum total cholesterol (TC) and triglyceride (TG) concentrations were observed in the SBS-supplemented group compared with the HFD group. We also found that the HFD supplemented with SBS group showed dramatically reduced hepatic lipid accumulation compared to the HFD alone group, and administration of SBS resulted in dramatic suppression of TG, TC in the HFD-induced fatty liver. In liver gene expression within the SBS treated group, PPARα was significantly increased and SREBP-1c was significantly suppressed. SBS induced a significant decrease in the hepatic mRNA levels of PPARγ, FAS, ACC1, and DGAT2. In conclusion, SBS improved cholesterol metabolism, decreased lipogenesis, and increased lipid oxidation in HFD-induced hepatic steatosis in rats, implying a potential application in treatment of non-alcoholic fatty liver disease.
    Nutrients 06/2014; 6(6):2179-2195. DOI:10.3390/nu6062179 · 3.15 Impact Factor