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本文研究了实验性高胆固醇血症大鼠肝脏低密度脂蛋白受体（ＬＤＬＲ）活性变化及有氧运动时ＬＤＬＲ活性调节的影响。发现，高脂（ＨＣ）组肝组织匀浆ＬＤＬＲ活性较正常对照（ＮＣ）组降低３７％（Ｐ＜０．０５），同时血清总胆固醇（ＴＣ）、低密度脂蛋白胆固醇（ＬＤＬＣ）及血清载脂蛋白Ｂ（ＡｐｏＢ）均显著高于ＮＣ组（Ｐ＜０．０１）；高脂＋运动（ＨＥ）组ＴＣ、ＬＤＬＣ及ＡｐｏＢ均明显低于ＨＣ组，而ＬＤＬＲ活性则较ＨＣ组增高２６％（Ｐ＜０．０５）。结果提示：（１）高胆固醇负荷时细胞可通过下行调节影响ＬＤＬＲ活性；（２）运动可能通过增加对细胞内胆固醇利用和降解，反馈作用于下行调节过程影响ＬＤＬＲ的合成，增加对ＬＤＬＣ摄取而显著改善血脂水平。
This article studies the experimental hypercholesterolemic rat liver low density lipoprotein receptor (LDL R activity changes and aerobic exercise LDL R activity regulation. The results showed that the activity of LDLR in the homogenate of the high fat (HC) group decreased 37% (P <0.05) compared with that of the normal control group (NC), while the levels of total cholesterol (TC), low density lipoprotein cholesterol C and serum apolipoprotein B (ApoB) were significantly higher than those in NC group (P <0.01). TC, LDL-C and ApoB in high fat + exercise group were significantly lower than those in HC group R activity increased by 26% compared with HC group (P <0.05). The results suggest that: (1) cells under high cholesterol load may affect LDL-R activity through down-regulation; (2) exercise may increase the LDL-R synthesis by increasing the effect on cholesterol utilization, degradation and feedback in cells, On the LDL C intake and significantly improve blood lipid levels.