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


METHODS
Male 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.


RESULTS
Although 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.


CONCLUSIONS
We 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.
Central Research Laboratory, Tokyo Innovation Center, Nippon Suisan Kaisha, Ltd,, 32-3 Nanakuni 1 Chome Hachioji, Tokyo 192-0991, Japan. yangzh@nissui.co.jp
Zhi-Hong
ZH
Yang
Hiroko
H
Miyahara
Jiro
J
Takeo
Akimasa
A
Hatanaka
Masashi
M
Katayama
D052242:Adiponectin / Q000097:blood; D000818:Animals; D004041:Dietary Fats / Q000009:adverse effects* / Q000032:analysis; D015536:Down-Regulation; D064429:Fatty Acid Synthases / Q000235:genetics / Q000378:metabolism; D005234:Fatty Liver / Q000209:etiology / Q000517:prevention & control*; D005395:Fish Oils / Q000737:chemistry / Q000627:therapeutic use*; D048388:Gadiformes; D006903:Hydroxymethylglutaryl CoA Reductases / Q000235:genetics / Q000378:metabolism; D006949:Hyperlipidemias / Q000097:blood / Q000178:diet therapy* / Q000209:etiology / Q000378:metabolism; D050152:Intra-Abdominal Fat / Q000378:metabolism; D020738:Leptin / Q000097:blood; D050356:Lipid Metabolism; D008099:Liver / Q000201:enzymology / Q000378:metabolism; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D012333:RNA, Messenger / Q000378:metabolism; D011897:Random Allocation; D052243:Resistin / Q000097:blood; D013230:Stearoyl-CoA Desaturase / Q000235:genetics / Q000378:metabolism; D051779:Sterol Regulatory Element Binding Proteins / Q000235:genetics / Q000378:metabolism
D052242:Adiponectin; C499919:Adipoq protein, mouse; D004041:Dietary Fats; D005395:Fish Oils; D020738:Leptin; D012333:RNA, Messenger; D052243:Resistin; C499623:Retn protein, mouse; D051779:Sterol Regulatory Element Binding Proteins; D006903:Hydroxymethylglutaryl CoA Reductases; C490333:Scd1 protein, mouse; D013230:Stearoyl-CoA Desaturase; D064429:Fatty Acid Synthases; C029310:lard