Effect of shunyo rice protein on cholesterol metabolism in adult rats | “春阳”大米蛋白对大鼠胆固醇代谢的调控作用

Китайский. 选用蛋白水平（CP）为14％的“春阳”大米蛋白（RP）、大豆蛋白（sP）、酪蛋白（CAS）为食物蛋白源，喂养雄性20周龄Wistar大鼠。经2周饲养后，各试验组间大鼠的生长性能、蛋白质功效无显著差异。与CAS组相比，RP及SP显著降低了大鼠血浆总胆固醇、血浆非高密度胆固醇（LDL-C、VLDL-C）水平及肝脏总脂质、肝脏胆固醇、肝脏甘油三酯含量。RP及SP显著阻碍大鼠的肠道胆固醇吸收，其肝脏胆固醇酯化率均显著低于CAS组。数据显示，RP显著刺激大鼠中性粪固醇、粪胆固醇的排泄，但大鼠粪胆汁酸的排泄与CAS组无显著差异。对比CAS，RP能够有效降低成熟期大鼠动脉硬化指数。结果表明，富含醇溶蛋白的“春阳”大米蛋白能够有效调控成熟期大鼠的胆固醇代谢，显示与大豆蛋白一致的降低机体胆固醇水平的作用效果，其主要作用机制之一是有效阻碍肠道胆固醇的吸收，而非单纯地刺激粪胆汁酸的排泄。[著者文摘]

Английский. To elucidate the effect of Shunyo rice protein,with high prolamin content,on cholesterol metabolism in adult rats. 20-week-old male Wistar rats were fed with Shunyo rice protein（RP）,soy protein（SP） and casein（CAS） ad libitum for 2 weeks（CP as 14%）, respectively. Similar growth performance and protein efficiency ratio were observed in all groups. Compared with CAS,RP and SP both produced marked hypocholesterolemic action, reflecting in the significant reduction of total cholesterol （TC）,low density lipoprotein cholesterol（LDL-C） and very low density lipoprotein cholesterol（VLDL- C） （P〈0.05） ,as a result,the atherogenic index（AI） of adult rats fed with RP was lower than those fed with CAS. The liver accumulations of total lipids, cholesterol（total cholesterol, free cholesterol and cholesterol ester） and triglyceride were significantly decreased in RP and SP when compared with CAS （P〈0.05）. The dramatic decrease of apparent cholesterol absorption（P〈0.05） and cholesterol esterifled ratio（P〈0.05） were also observed both in this study. The similar stimulation in excretion of fecal neutral sterol and fecal cholesterol were observed both in adult rats fed with RP and SP（P〈0. 05）. SP increased fecal bile acids excretion,whereas RP did not. Results suggested that Shunyo rice protein,with high prolamin content, efficaciously lowered plasma and liver cholesterol level in adult rats, showing a similar cholesterol-lowering effect with soy protein. The mechanism of cholesterol-lowering effects induced by Shunyo rice protein cannot be explained by the result of a simple diversion of bile acids toward fecal excretion. Inhibition of intestinal cholesterol absorption may be the primary mechanism due to the poor digestibility of prolamin.