Pollock oil supplementation modulates hyperlipidemia and ameliorates hepatic steatosis in mice fed a high-fat diet

Abstract

BackgroundHyperlipidemia associated with obesity is closely related to the development of atherosclerosis. Both n-3 polyunsaturated fatty acids (PUFAs) and long-chain monounsaturated fatty acids (MUFAs; i.e., C20:1 and C22:1 isomers) supplementation modulate risk factors for metabolic syndrome via multiple mechanisms, including the restoration of impaired lipid metabolism. We therefore examined the effects of pollock oil, which contains a considerable amount of n-3 PUFAs as well as long-chain MUFAs, on plasma hyperlipidemia and hepatic steatosis in diet-induced obese mice.MethodsMale C57BL/6J mice (24-26 g) were divided into two groups (n = 10/group) and were fed a high-fat diet containing 32% lard (control group) or 17% lard plus 15% pollock oil (experimental group) for 6 weeks. For both groups, fat comprised 60% of the total caloric intake.ResultsAlthough body and liver masses for the two groups did not differ significantly, hepatic lipids concentrations (triglycerides and total cholesterols) were lower (P < 0.05) after pollock oil ingestion. After 2 weeks on the specified diets, plasma lipid levels (total cholesterol, LDL cholesterol, and triglycerides) significantly decreased (P < 0.05) in the experimental group compared with the control group, although plasma HDL cholesterol levels did not differ. At the end of 6 weeks, plasma adiponectin levels increased (P < 0.05), whereas plasma resistin and leptin levels decreased (P < 0.05) in the experimental mice. Increased levels of long-chain MUFAs and n-3 PUFAs in plasma, liver and adipose tissue by ingesting pollock oil were possibly correlated to these favorable changes. Expression of hepatic genes involved in cholesterol metabolism (SREBP2, HMGCR, and ApoB) and lipogenesis (SREPB1c, SCD-1, FAS, and Acacα) was suppressed in the experimental group, and may have favorably affected hyperlipidemia and hepatic steatosis induced by the high-fat diet.ConclusionsWe demonstrated that pollock oil supplementation effectively improved hyperlipidemia, attenuated hepatic steatosis, and downregulated the express of hepatic genes involved in cholesterol and lipid metabolism in mice with diet-induced obesity.

Potential protective effect of Nigella sativa crude oils towards fatty liver in rats

“…These results suggest that palmitoleate, in addition to eicosapentaenoic acid, play a role in the regulation of lipid metabolism by fish oil . Administration of pollock oil, which contains a considerable amount of n −3 polyunsaturated fatty acids as well as long‐chain MUFAs effectively improved hyperlipidemia and attenuated hepatic steatosis, in obese mice .…”

Dietary marine-derived long-chain monounsaturated fatty acids and cardiovascular disease risk: a mini review

“…Suppression of genes related to adipogenesis and induction of genes involved in fatty acid oxidation and insulin signaling with saury oil supplementation were also associated with improvements in glucose and lipid metabolism. Similarly, 6-week treatment of 15% ( w/w ) of LCMUFA-rich pollock oil (equivalent to appropriate 3.9% ( w/w ) LCMUFA) in diet-induced obese mice increased organ levels of LCMUFA, and suppressed the rise in proatherogenic LDL-cholesterol without decreasing anti-atherogenic levels of HDL-cholesterol [35]. An attenuation in hepatic steatosis and a down-regulation of hepatic genes involved in cholesterol and lipid synthesis by the pollock oil diet most likely contributed to these findings.…”

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

“…It is well established that amelioration of lipid concentration in the blood prevents hypercholesterolemia and hepatic lipid accumulation. Lipid metabolism in the liver is controlled by fatty acid-synthesizing and energy expenditure enzymes, with decreased energy expenditure enzymes and increased fatty acid-synthesizing enzymes generally being observed in the livers of obese animal models fed a high-fat diet (HFD) and/or a high-cholesterol diet (HCD) (2,(7)(8)(9). Furthermore, the hepatic expression levels of LDL receptor (LDLR) are associated with the concentration of circulating serum cholesterol in experimental animals fed a HFD and/or HCD (10).…”