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.
出处
《营养学报》
CAS
CSCD
北大核心
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)