Russell J C, Koeslag D G, Amy R M, Dolphin P J
Department of Surgery, University of Alberta, Edmonton, Canada.
Arteriosclerosis. 1989 Nov-Dec;9(6):869-76. doi: 10.1161/01.atv.9.6.869.
The JCR:LA-corpulent rat is an obese, hyperlipidemic, hyperinsulinemic strain that is atherosclerosis-prone and develops myocardial lesions. The hyperlipidemia is due to elevated plasma levels of a large relatively triglyceride-rich very low density lipoprotein (VLDL). Both corpulent and lean male and female rats were studied. Postheparin lipid clearance and apparent hepatic secretion rate after Triton WR1339 inhibition of lipoprotein lipase were determined. The concentrations of cholesterol and cholesteryl esters were not significantly altered by either treatment. Triglycerides showed rapid postheparin clearance in corpulent rats. The apparent hepatic secretion rate was markedly higher in corpulent male rats than in lean male rats, and the rate in corpulent females was again higher, reflecting the higher serum triglyceride concentrations in corpulent female rats. The relative secretion rate of C:48 triglyceride molecular species was lower than that of the C:50 to C:56 species, while the postheparin clearance of C:48 triglyceride molecular species was impaired compared to the C:50 species and those with higher carbon numbers. This effect was more marked in the male than in the female corpulent rats. The results indicate that VLDL hyperlipidemia in the corpulent rat is due to hepatic hypersecretion of VLDL and not to a defect in lipoprotein lipase. Further, the atherogenesis that is characteristic of the corpulent male rat may be related to the differential metabolism of fatty acids.
LA肥胖大鼠是一种肥胖、高脂血症、高胰岛素血症的品系，易患动脉粥样硬化并会出现心肌病变。高脂血症是由于血浆中一种相对富含甘油三酯的大颗粒极低密度脂蛋白（VLDL）水平升高所致。对肥胖和瘦的雄性及雌性大鼠均进行了研究。测定了注射肝素后的脂质清除率以及经曲拉通WR1339抑制脂蛋白脂肪酶后的肝脏表观分泌率。两种处理均未显著改变胆固醇和胆固醇酯的浓度。肥胖大鼠注射肝素后甘油三酯清除迅速。肥胖雄性大鼠的肝脏表观分泌率明显高于瘦雄性大鼠，肥胖雌性大鼠的该分泌率更高，这反映出肥胖雌性大鼠血清甘油三酯浓度更高。C:48甘油三酯分子种类的相对分泌率低于C:50至C:56的种类，而与C:50种类及碳数更高的种类相比，C:48甘油三酯分子种类的注射肝素后清除受损。这种效应在肥胖雄性大鼠中比在肥胖雌性大鼠中更明显。结果表明，肥胖大鼠的VLDL高脂血症是由于肝脏VLDL分泌过多，而非脂蛋白脂肪酶缺陷所致。此外，肥胖雄性大鼠特有的动脉粥样硬化形成可能与脂肪酸的差异代谢有关。
