Wergedahl Hege, Gudbrandsen Oddrun Anita, Røst Therese Halvorsen, Berge Rolf Kristian
The Lipid Research Group, Institute of Medicine, Section of Medical Biochemistry, University of Bergen, Bergen, Norway.
Nutrition. 2009 Jan;25(1):98-104. doi: 10.1016/j.nut.2008.07.005. Epub 2008 Aug 26.
This study investigated the potential additive or synergistic effect of fish oil (FO) and fish protein hydrolysate (FPH) on cholesterol concentration in plasma and the liver.
Male Wistar rats were fed high-fat diets (30% fat, 20% protein, wt/wt) containing FO (5%), FPH (10%), a combination of FO and FPH, or a high-fat control diet. After 7 wk of feeding, the rats were fasted for 12 h before lipid levels in plasma and the liver and hepatic activities of acyl-coenzyme A:cholesterol acyltransferase, 3-hydroxy-3-methylglutaryl coenzyme A reductase, and fatty acid synthase were measured.
The combination of FO and FPH in the diet profoundly reduced the plasma cholesterol level, mainly due to lowering of high-density lipoprotein cholesterol, whereas the hepatic total cholesterol concentration was elevated compared with control rats and rats fed diets containing FPH or FO alone. The elevated cholesterol concentration in the liver was caused by an increased amount of cholesteryl esters and was in correlation to an increased activity of acyl-coenzyme A:cholesterol acyltransferase. There was a reduced fatty acid synthase activity that could lead to a reduced lipogenesis in the rats fed a combination of FO and FPH.
A dietary combination of FO and FPH resulted in lower levels of plasma cholesterol and higher levels of hepatic cholesterol compared with dietary FO or FPH alone. Further studies are warranted to confirm whether the hypocholesterolemic effect was due to a reduced secretion of very low-density lipoprotein from the liver.
本研究调查了鱼油(FO)和鱼蛋白水解物(FPH)对血浆和肝脏中胆固醇浓度的潜在相加或协同作用。
将雄性Wistar大鼠喂食含FO(5%)、FPH(10%)、FO与FPH组合的高脂饮食(30%脂肪,20%蛋白质,重量/重量)或高脂对照饮食。喂食7周后,大鼠在测量血浆和肝脏中的脂质水平以及酰基辅酶A:胆固醇酰基转移酶、3-羟基-3-甲基戊二酰辅酶A还原酶和脂肪酸合酶的肝脏活性之前禁食12小时。
饮食中FO和FPH的组合显著降低了血浆胆固醇水平,主要是由于高密度脂蛋白胆固醇降低,而与对照大鼠以及单独喂食含FPH或FO饮食的大鼠相比,肝脏总胆固醇浓度升高。肝脏中胆固醇浓度升高是由胆固醇酯量增加引起的,并且与酰基辅酶A:胆固醇酰基转移酶活性增加相关。在喂食FO和FPH组合的大鼠中,脂肪酸合酶活性降低,这可能导致脂肪生成减少。
与单独的饮食FO或FPH相比,饮食中FO和FPH的组合导致血浆胆固醇水平降低,肝脏胆固醇水平升高。有必要进一步研究以确认降胆固醇作用是否归因于肝脏极低密度脂蛋白分泌减少。