Dietary n-3 polyunsaturated fatty acids decrease hepatic triglycerides in Fischer 344 rats

Abstract

Dietary fatty acid composition modifies hepatic lipid metabolism. To determine the effects of fatty acids on hepatic triglyceride storage, rats were fed diets enriched in carbohydrates (control), fish oil, or lard. After 4 weeks, the animals were fasted overnight. In the morning, the animals were either sacrificed or fed 8 g of their respective diets before sacrifice. Animals ingested more food calories with diets containing fish oil than with other diets. However, fish oil-fed animals weighed less and had less body fat. In fish oil-fed animals, liver triglyceride was lower by 27% (P < .05) and 73% (P < .01) than in control-and lard-fed animals, respectively. Fish oil altered the postprandial gene expression of hepatic regulators of fatty acid degradation and synthesis. Fish oil feeding blunted the normal postprandial decline in fatty acid degradation genes (PPAR␣, CPT1, and ACO) and blunted the normal postprandial rise in triglyceride synthesis genes (SREBP1-c, FAS, SCD-1). Therefore, the direct postprandial effect of fish oil ingestion decreases the propensity for hepatic triglyceride storage. In conclusion, n-3 polyunsaturated fatty acids decrease total body weight, total body fat, and hepatic steatosis. (HEPATOLOGY 2004;39:608 -616.)

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

“…In Fisher 344 rats, those fed a large amount of lard (45 en%) showed 3.7-fold greater hepatic TG concentration than those fed a large amount of fish oil (45 en%). 26 The postprandial TG concentration in lard-fed rats was 221 mg/dL, whereas that in fish oil-fed rats was 75 mg/dL, suggesting that the increased amount of absorbed fat may be responsible for TG accumulation in the liver. 26 In experiment II, we also observed increased postprandial TG concentration in high-butterfed and high-safflower oil-fed mice (relative to highstarch-fed mice); however, fish oil slightly inhibited this Table 2.…”

Novel aspects of PPARα-mediated regulation of lipid and xenobiotic metabolism revealed through a nutrigenomic study

“…However, in PPAR␣ Ϫ/Ϫ mice fed SUN, LIN, and FISH diets, TG accumulation was reduced, which is consistent with the beneficial effect of PUFAs on hepatic steatosis reported in other rodent models. 19,21,22 The absence of an effect of the REF diet in PPAR␣ Ϫ/Ϫ mice further suggests that when the hepatic FA sensor PPAR␣ is compromised, some PUFAs can achieve their beneficial effect only when they have reached a critical threshold rate in the diet. Remarkably, in our study, the replacement of 15% of the fat with fish oil (FISH vs. REF) led to a significant reduction of hepatic FA accumulation in both genotypes.…”

Prevention of reperfusion injury and microcirculatory failure in macrosteatotic mouse liver by omega-3 fatty acids

“…Conversely, n-3 PUFAs downregulate steroid-responsive element binding protein 1-c, which increases transcription of genes responsible for fatty acid synthesis such as fatty acid synthase and stearoyl Co-A desaturase. 28 Dietary provision of n-3 PUFAs via fish oil modulates the fatty acid composition of cell membrane phospholipids 29 and reduces intrahepatic lipid accumulation as well as the percentage of big fat droplets and therefore improves microcirculation. 20 In ob/ob mice, n-3 PUFA supplementation resulted in conversion of hepatic macrosteatosis to microsteatosis with a change of n-6:n-3 PUFA ratio to approach that of lean livers.…”