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为从脂蛋白胆固醇代谢的分子受体水平探讨胆囊胆固醇结石的成因，作者采用高胆固醇膳食建立兔胆囊胆固醇结石模型，而后对进食高胆固醇膳食后１、２、３、４周组及对照组肝细胞低密度脂蛋白（ＬＤＬ）受体活性变化进行了动态研究。结果发现：高胆固醇膳食后１周开始出现胆囊结石，２、３、４周组分别有４／１０、６／１０和７／１０只兔出现胆囊结石；１２５Ｉ－ＬＤＬ与肝细胞ＬＤＬ受体最大结合力在１周组略升高（Ｐ＞０．０５），２周组逐渐下降，３周和４周组明显下降（Ｐ＜０．０５）；解离常数Ｋｄ值逐渐升高，以３周和４周组明显（Ｐ＜０．０５）。由此提示：随着高胆固醇膳食进食时间延长，肝细胞ＬＤＬ受体活性下降，致血清ＬＤＬ清除受阻和胆汁中胆酸减少，可能在胆囊胆固醇结石形成过程中起着重要作用。
In order to explore the genesis of gallstone gallstone from the molecular level of lipoprotein cholesterol metabolism, the author used high cholesterol diet to establish the model of gallbladder gallstone in rats, and then the rats in 1, 2, 3, 4 weeks after high cholesterol diet and control group Dynamic changes of cell low density lipoprotein (LDL) receptor activity were studied. The results showed that gallstone started to appear at 1 week after high cholesterol diet, and gallbladder stones appeared in 4, 10, 6/10, and 7/10 rabbits in groups 2, 3, and 4, respectively. 125I-LDL and hepatocyte LDL receptors were the largest The binding capacity increased slightly in the first week (P> 0.05), decreased gradually in the second week, decreased obviously in the third week and the fourth week (P <0.05), and the dissociation constant Kd increased gradually to 3 Weeks and 4 weeks group was significantly (P <0.05). This suggests that: with high cholesterol dietary intake of prolonged liver LDL receptor activity decreased, resulting in obstruction of serum LDL and bile cholic acid reduction may play an important role in gallstone gallstone formation.