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: 2.91).
11/2011; 59(24):13353-9. DOI: 10.1021/jf203761t
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.
Available from: Zhengxing Lian
- "In general, cholesterol is indispensable to the human body, and its levels are subjected to complex regulation. Cholesterol is modified into oxysterols, including 22-and 24-hydroxy cholesterol, when excess cholesterol is deposited in hepatic cells (Satoshi Hirako et al., 2011). As expected , we demonstrated that the high-cholesterol diet increased hepatic TC, TG and LDL-C levels in rats (Table 2). "
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ABSTRACT: To investigate the effects of Kluyveromyces marxianus M3 isolated from Tibetan mushrooms on diet-induced hypercholesterolemia in rats, female Wistar rats were fed a high-cholesterol diet (HCD) for 28 d to generate hyperlipidemic models. Hyperlipidemic rats were assigned to four groups, which were individually treated with three different dosages of K. marxianus M3+HCD or physiological saline+HCD via oral gavage for 28 d. The total cholesterol (TC), triglycerides (TG), high-density lipoprotein cholesterol (HDL-C), and low-density lipoprotein cholesterol (LDL-C) levels in the serum and liver of the rats were measured using commercially available enzyme kits. In addition, the liver morphology was also examined using hematoxylin and eosin staining and optical microscopy. According to our results, the serum and liver TC, TG, LDL-C levels and atherogenic index (AI) were significantly decreased in rats orally administered K. marxianus M3 (p <0.01), and the HDL-C levels and anti atherogenic index (AAI) were significantly increased (p <0.01) compared to the control group. Moreover, K. marxianus M3 treatment also reduced the build-up of lipid droplets in the liver and exhibited normal hepatocytes, suggesting a protective effect of K. marxianus M3 in hyperlipidemic rats.
06/2015; 46(2):389-95. DOI:10.1590/S1517-838246220131278
Available from: Kei Nakajima
- "Enjoji and Nakamuta  proposed that excess cholesterol intake appears to be one of the main factors associated with NAFLD, particularly in nonobese subjects, because excess cholesterol consumption stimulates the liver X receptor-α–SREBP-1c pathway and enhances fatty acid synthesis. Indeed, it was reported that low-dose (2.0% of total energy) fish oil diets improve hepatic lipid accumulation in mice fed a high-cholesterol diet . However, studies examining the effects of EPA/fish oil on dietary cholesterol-induced NAFLD in humans are still lacking. "
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ABSTRACT: Nonalcoholic fatty liver disease (NAFLD) and non-alcoholic steatohepatitis (NASH) are multidisciplinary liver diseases that often accompany type 2 diabetes or metabolic syndrome, which are characterized by insulin resistance. Therefore, effective treatment of type 2 diabetes and metabolic syndrome should target not only the cardiometabolic abnormalities, but also the associated liver disorders. In the last decade, it has been shown that metformin, thiazolidinediones, vitamin E, ezetimibe, n-3 polyunsaturated fatty acids, renin-angiotensin system (RAS) blockers, and antiobesity drugs may improve hepatic pathophysiological disorders as well as clinical parameters. Accordingly, insulin sensitizers, antioxidative agents, Niemann-Pick C1-like 1 (NPC1L1) inhibitors, RAS blockers, and drugs that target the central nervous system may represent candidate pharmacotherapies for NAFLD and possibly NASH. However, the efficacy, safety, and tolerability of long-term treatment (potentially for many years) with these drugs have not been fully established. Furthermore, clinical trials have not comprehensively examined the efficacy of lipid-lowering drugs (i.e., statins, fibrates, and NPC1L1 inhibitors) for the treatment of NAFLD. Although clinical evidence for RAS blockers and incretin-based agents (GLP-1 analogs and dipeptidyl peptidase-4 inhibitors) is also lacking, these agents are promising in terms of their insulin-sensitizing and anti-inflammatory effects without causing weight gain.
12/2012; 2012(8):950693. DOI:10.1155/2012/950693
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ABSTRACT: Fatty liver induced by alcohol abuse is a major worldwide health hazard leading to morbidity and mortality. Previous studies indicate anti-fatty liver properties of garlic. In this study we have investigated the molecular mechanisms of garlic oil (GO) or diallyl disulfide (DADS) imparted hepatoprotection against alcohol induced fatty liver in C57BL/6 mice using microarray-based global gene expression analysis. Alcohol liquid diet resulted in severe fatty liver with increased levels of serum aspartate aminotransferease and alanine aminotransferease, triglycerides and decreased levels of liver glutathione and antioxidant enzymes. The major canonical pathways implicated by alcohol treatment are the metabolisms of xenobiotics by cytochrome P450, glutathione and arachidonic acid. Treatment with DADS or GO normalized the serum aminotransferease levels, liver antioxidant enzymes and reduced the contents of triglycerides and cholesterol. The canonical pathways involved in the amelioration of liver includes arachidonic acid metabolism, altered T cell and B cell signaling, tryptophan metabolism, and antigen presentation pathway for DADS; and metabolism of xenobiotics, mitotic roles of Polo-like kinase, fatty acid metabolism, LPS/IL-1 mediated inhibition of RXR function, and C21-steroid hormone metabolism for GO.
Journal of Agricultural and Food Chemistry 10/2012; 60(44). DOI:10.1021/jf303800p · 2.91 Impact Factor
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