Central Research Laboratory, Tokyo Innovation Center, Nippon Suisan Kaisha, Ltd,, 32-3 Nanakuni 1 Chome Hachioji, Tokyo 192-0991, Japan.
Lipids Health Dis. 2011 Oct 25;10:189. doi: 10.1186/1476-511X-10-189.
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.
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.
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.
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.
肥胖相关的高血脂与动脉粥样硬化的发展密切相关。n-3 多不饱和脂肪酸(PUFAs)和长链单不饱和脂肪酸(MUFAs;即 C20:1 和 C22:1 异构体)补充剂通过多种机制调节代谢综合征的危险因素,包括恢复受损的脂质代谢。因此,我们研究了富含 n-3 PUFAs 和长链 MUFAs 的狭鳕鱼油对饮食诱导肥胖小鼠的血浆高血脂和肝脂肪变性的影响。
雄性 C57BL/6J 小鼠(24-26 g)分为两组(每组 n = 10),并分别喂食含有 32%猪油(对照组)或 17%猪油加 15%狭鳕鱼油(实验组)的高脂肪饮食 6 周。两组的脂肪均占总热量摄入的 60%。
尽管两组的体重和肝重没有显著差异,但摄入狭鳕鱼油后肝内脂质浓度(甘油三酯和总胆固醇)较低(P < 0.05)。在特定饮食 2 周后,实验组的血浆脂质水平(总胆固醇、LDL 胆固醇和甘油三酯)显著降低(P < 0.05),而血浆 HDL 胆固醇水平没有差异。6 周结束时,实验组血浆脂联素水平升高(P < 0.05),而血浆抵抗素和瘦素水平降低(P < 0.05)。摄入狭鳕鱼油后,血浆、肝脏和脂肪组织中长链 MUFAs 和 n-3 PUFAs 水平升高,可能与这些有利变化有关。实验组肝脏胆固醇代谢(SREBP2、HMGCR 和 ApoB)和脂肪生成(SREPB1c、SCD-1、FAS 和 Acacα)相关基因的表达受到抑制,可能有利于改善高脂肪饮食引起的高血脂和肝脂肪变性。
我们证明了狭鳕鱼油补充剂可有效改善饮食诱导肥胖小鼠的高血脂,减轻肝脂肪变性,并下调肝脏胆固醇和脂质代谢相关基因的表达。