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采用高胆固醇膳食诱发兔胆囊胆固醇结石模型，分别对高胆固醇膳食后１、２、３、４周及对照组高密度脂蛋白受体（ Ｈ Ｄ Ｌｒ）活性，胆汁中胆汁酸及胆固醇变化进行了研究。结果发现：①高胆固醇膳食后１周肝细胞 Ｈ Ｄ Ｌｒ Ｂｍ ａｘ 明显增大而 Ｋｄ 值明显变小，与对照组相比有显著性差异（ Ｐ＜ ０．０５），２周组两者降至对照组水平，３周及４周组 Ｂｍ ａｘ 明显变小而 Ｋｄ 值明显增大，有显著性差异（ Ｐ＜ ０．０５），②１周组胆汁中总胆汁酸含量增加，２周组与对照组相近，３周组胆汁酸含量减少（ Ｐ＞ ０．０５），４周组则明显减少（ Ｐ＜ ０．０５）；③随着高胆固醇膳食进食时间增加，胆汁中胆固醇含量持续增加，３周组及４周组与对照组有显著性差异（ Ｐ＜ ０．０５）。成石中肝细胞 Ｈ Ｄ Ｌｒ 活性及胆汁中胆汁酸含量均表现为先升后降，提示肝细胞 Ｈ Ｄ Ｌｒ 活性下降可能引起 肝细胞摄取用于胆汁酸合成的底物减少，并可能在胆囊结石形成中起重要作用。
Cholesterol gallstone induced by hypercholesterolemia in rabbits was induced by hypercholesterolemia. The changes of high density lipoprotein receptor (H D Lr), bile acid and cholesterol in bile the study. The results showed that: (1) H D Lr Bm ax of hepatocytes increased significantly and Kd value decreased significantly at 1 week after hypercholesterolemia, which was significantly different from that of control group (P <0.05) (P <0.05). (2) The levels of total bile acid in bile in 1 week group were significantly increased, and the levels of total bile acid in 2 weeks and 2 weeks group were significantly lower than those in control group Compared with the control group, the content of bile acid decreased in 3 weeks (P> 0.05) and decreased significantly in 4 weeks (P <0.05). ③ With the increase of high cholesterol dietary intake, the content of cholesterol in bile continued to increase, 3 weeks group and 4 weeks group and control group have significant difference (P <0.05). H D Lr activity in liver cells and bile acid content in bile were all increased first and then decreased, suggesting that the decrease of H D Lr activity in hepatocytes may lead to the decrease of substrate for hepatocyte uptake for bile acid synthesis, Stone formation plays an important role.