Fantappiè S, Catapano A L, Cancellieri M, Fasoli L, De Fabiani E, Bertolini M, Bosisio E
Institute of Pharmacological Sciences, University of Milan, Italy.
Life Sci. 1992;50(24):1913-24. doi: 10.1016/0024-3205(92)90552-z.
The purpose of this study was to characterize the lipoprotein profile and cholesterol metabolism in Yoshida rats, a strain of inbred genetically hyperlipemic animals. For comparison, Brown Norway rats were used as control animals. Plasma cholesterol and triglycerides were higher in Yoshida as compared to Brown Norway, the elevation of cholesterol being due to a rise in HDL fraction. Triglyceride distribution among lipoproteins showed an increase in VLDL fraction. Hyperlipemia was not related to diabetes, hypothyroidism or nephropathy. Plasma triglycerides production was increased in Yoshida rats, while lipoprotein and hepatic lipases were similar in the two groups. Hypercholesterolemia was associated with a defect of lipoprotein receptor activity and with elevated HMG-CoA reductase and cholesterol 7 alpha - hydroxylase; conversely ACAT activity was lower in Yoshida as compared to Brown Norway rats. Sterol fecal excretion was comparable in the two groups and hypercholesterolemia in Yoshida rats was not associated to an increase of cholesterol saturation of the bile. We suggest that lipoprotein overproduction is the main cause for hyperlipidemia in this strain of rats.
本研究的目的是描述吉田大鼠（一种近交系遗传性高脂血症动物品系）的脂蛋白谱和胆固醇代谢特征。作为对照，选用了棕色挪威大鼠。与棕色挪威大鼠相比，吉田大鼠血浆胆固醇和甘油三酯水平更高，胆固醇升高是由于高密度脂蛋白（HDL）部分增加所致。甘油三酯在脂蛋白中的分布显示极低密度脂蛋白（VLDL）部分增加。高脂血症与糖尿病、甲状腺功能减退或肾病无关。吉田大鼠血浆甘油三酯生成增加，而两组的脂蛋白脂肪酶和肝脂肪酶相似。高胆固醇血症与脂蛋白受体活性缺陷以及3-羟基-3-甲基戊二酰辅酶A（HMG-CoA）还原酶和胆固醇7α-羟化酶升高有关；相反，与棕色挪威大鼠相比，吉田大鼠的酰基辅酶A：胆固醇酰基转移酶（ACAT）活性较低。两组的粪便固醇排泄相当，吉田大鼠的高胆固醇血症与胆汁胆固醇饱和度增加无关。我们认为脂蛋白生成过多是该品系大鼠高脂血症的主要原因。
