高脂膳食对SR-AⅠ/Ⅱ基因缺失小鼠脂代谢的影响  

EFFECTS OF HIGH-FAT DIET ON LIPID METABOLISM IN SR-AⅠ/Ⅱ GENE KNOCK-OUT MICE

作　　者：麦海妍[1,2] 夏颖[2] 凌文华[2] 

机构地区：[1]中山大学附属第一医院营养科 [2]中山大学公共卫生学院营养系,广州510080

出　　处：《营养学报》2009年第5期441-446,共6页Acta Nutrimenta Sinica

基　　金：国家自然科学基金(No.30571568)

摘　　要：目的探讨A类Ⅰ型和Ⅱ型清道夫受体(scavenger receptor class A typesⅠandⅡ,SR-AⅠ/Ⅱ)基因缺失对高脂膳食小鼠脂质代谢的影响及其可能的作用机制。方法以SR-AⅠ/Ⅱ基因敲除与野生型雄性小鼠为对象,分别喂饲普通膳食和高脂膳食12w,应用酶法或油红O染色法检测脂质代谢(包括血脂水平和肝脏脂质水平)的变化,采用RT-PCR法检测肝脏B类Ⅰ型清道夫受体(scavenger receptor class B typeⅠ,SR-BⅠ)和CD36的表达。结果SR-AⅠ/Ⅱ基因敲除鼠与野生型鼠相比,高脂膳食喂饲的第3、6、12w,其血清TG、TC、LDL、HDL均比野生型小鼠下降,肝细胞中脂滴的数量较多,体积较大,SR-BⅠmRNA表达上调,CD36mRNA的表达无差异。结论高脂膳食诱导SR-AⅠ/Ⅱ基因缺失小鼠脂质代谢的变化可能与肝脏SR-BⅠ表达升高及外周脂质向肝脏的逆向转运有关。Objective To observe the alteration of scavenger receptor class A types Ⅰ and Ⅱ （SR-A Ⅰ /Ⅱ ） gene knock-out on lipid metabolism in mice fed with high-fat diet, and explore the underlying mechanism. Method The SR-A Ⅰ/Ⅱ gene knock-out and wild-type male mice were fed with normal and high-fat diet for 12 w. Thereafter, the level of lipid metabolism （such as the levels of lipids in blood and liver） was detected with enzyme method or oil red O staining, and the expression of scavenger receptor class B type Ⅰ （SR-B Ⅰ ） and CD36 in liver was analyzed by RT-PCR. Results Under high-fat diet condition, as compared with wild-type mice, the levels of TG, TC, LDL and HDL in SR-A Ⅰ / Ⅱ gene knock-out mice were decreased at 3, 6, 12 w （P〈0.05）. The number of lipid droplets in liver was more and the volume was larger. Furthermore, the expression of SR-B ⅠmRNA was higher, but the expression of CD36 mRNA was not obviously different （P〉0.05）. Conclusion The alteration of lipid metabolism induced by high-fat diet in SR-A Ⅰ /Ⅱ gene knock-out mice might be relative with the up-regulated SR-B Ⅰ mRNA expression and the counter transport of peripheral lipids to liver.

关 键 词：A类清道夫受体 脂质 B类Ⅰ型清道夫受体 CD36 

分 类 号：R151[医药卫生—营养与食品卫生学]