Fish oil prevents sucrose-induced fatty liver but exacerbates high-safflower oil-induced fatty liver in ddy mice

Abstract

Diets high in sucrose/fructose or fat can result in hepatic steatosis (fatty liver). We analyzed the effects of dietary fish oil on fatty liver induced by sucrose, safflower oil, and butter in ddY mice. In experiment I, mice were fed a high-starch diet [70 energy% (en%) starch] plus 20% (wt/wt) sucrose in the drinking water or fed a high-safflower oil diet (60 en%) for 11 weeks. As a control, mice were fed a high-starch diet with drinking water. Fish oil (10 en%) was either supplemented or not. Mice supplemented with sucrose or fed safflower oil showed a 1.7-fold or 2.2-fold increased liver triglyceride content, respectively, compared with that of control mice. Fish oil completely prevented sucrose-induced fatty liver, whereas it exacerbated safflower oil-induced fatty liver. Sucrose increased SREBP-1c and target gene messenger RNAs (mRNAs), and fish oil completely inhibited these increases. In experiment II, mice were fed a high-safflower oil or a high-butter diet, with or without fish oil supplementation. Fish oil exacerbated safflower oilinduced fatty liver but did not affect butter-induced fatty liver. Fish oil increased expression of peroxisome proliferator-activated receptor gamma (PPAR␥) and target CD36 mRNA in safflower oil-fed mice. These increases were not observed in sucrose-supplemented or butter-fed mice. Conclusion: The effects of dietary fish oil on fatty liver differ according to the cause of fatty liver; fish oil prevents sucrose-induced fatty liver but exacerbates safflower oil-induced fatty liver. The exacerbation of fatty liver may be due, at least in part, to increased expression of liver PPAR␥.

The ddY mouse: a model of postprandial hypertriglyceridemia in response to dietary fat

“…As suggested by our previous studies (18)(19)(20), a marked increase in postprandial TG concentrations after being fed a HF diet was observed in ddY mice but not in C57BL/6J mice. Mice were fed a standard laboratory chow and fasted for 24 h and then allowed to freely eat a HF diet (60% energy from saffl ower oil).…”

“…by guest, on March 28, 2019 www.jlr.org Downloaded from in the SREBP-1c promoter and show hepatic steatosis when fed sucrose supplementation or a HF diet ( 19 ). Mice with guanine at this site show increased liver SREBP-1c mRNA in response to a high-fructose diet, whereas mice with adenine, such as C57BL/6J mice, do not ( 47 ).…”

Comparative Effects of Sesame Seeds Differing in Lignan Contents and Composition on Fatty Acid Oxidation in Rat Liver

“…This may be due to the up-regulation of Cd36, which mediates fatty acid uptake from the circulation. Studies in mice 25,47 indicated that Cd36 plays a crucial role in the transport of fatty acid in hepatocytes and hence regulates the hepatic triacylglycerol concentration. We previously observed that sesame lignan decreased hepatic concentration of triacylglycerol in rats fed a saturated fat palm oil 16,48,49 .…”

Eicosapentaenoic acid attenuates hepatic accumulation of cholesterol esters but aggravates liver injury and inflammation in mice fed a cholate-supplemented high-fat diet

“…These actions have been shown to be mediated through the downregulation of SREBP-1 expression (Sekiya et al, 2003;Yamazaki et al, 2007). In addition, it is reported that PUFA can suppress SOAT-2 expression in experimental animals (Botham et al, 2001;Lecker et al, 2011).…”

“…Notably, the oleic acid (18:1n-9)-containing CE level was markedly elevated in the liver of mice fed the CAHF diet compared with in the liver of those fed the normal diet (Watanabe and Tsuneyama, 2012). On the other hand, the administration of fish oil or its major n-3 polyunsaturated fatty acids (PUFA) is effective in attenuating hepatic steatosis in experimental animals (Hein et al, 2010;Jung et al, 2011;Kajikawa et al, 2009;Sekiya et al, 2003;Tanaka et al, 2010;Yamazaki et al, 2007). Moreover, n-3 PUFA administration could prevent the hepatic accumulation of TG through the suppression of monounsaturated fatty acids (MUFA) generation (Kajikawa et al, 2009).…”