Maggio C A, Greenwood M R
Physiol Behav. 1982 Dec;29(6):1147-52. doi: 10.1016/0031-9384(82)90312-2.
To investigate the relationship between elevated adipose tissue lipoprotein lipase (LPL) activity and triglyceride uptake in Zucker obese rats, fed and 12 hour fasted female obese and lean Zucker rats were given intrajugular infusion of radio-labelled triglyceride and label clearance and uptake were examined over 35 minutes. In the fed state, obese rats showed more rapid clearance of the label from the bloodstream and, in both fed and fasted states, greater uptake into retroperitoneal and parametrical fat pads than lean rats. Obese rats showed proportionally less uptake into heart and liver. Regardless of feeding condition, obese rats exhibited elevations in adipose tissue LPL, which was significantly correlated with label uptake in adipose tissue. These results show that, in Zucker obese rats, elevated adipose tissue LPL is associated with increased adipose tissue triglyceride uptake. A preferential "shunting of calories" into adipose tissue, which is presumably mediated by LPL, could underlie the intractability of the Zucker obesity syndrome as well as the altered feeding behavior of Zucker obese rats.
为了研究脂肪组织脂蛋白脂肪酶（LPL）活性升高与 Zucker 肥胖大鼠甘油三酯摄取之间的关系，对进食及禁食 12 小时的雌性肥胖和瘦 Zucker 大鼠进行颈内静脉注射放射性标记的甘油三酯，并在 35 分钟内检测标记物的清除和摄取情况。在进食状态下，肥胖大鼠的标记物从血液中的清除速度更快，并且在进食和禁食状态下，与瘦大鼠相比，其腹膜后和子宫旁脂肪垫的摄取量更大。肥胖大鼠心脏和肝脏的摄取量相对较少。无论进食情况如何，肥胖大鼠脂肪组织中的 LPL 都会升高，这与脂肪组织中标记物的摄取显著相关。这些结果表明，在 Zucker 肥胖大鼠中，脂肪组织 LPL 升高与脂肪组织甘油三酯摄取增加有关。热量优先“分流”到脂肪组织中，这可能是由 LPL 介导的，可能是 Zucker 肥胖综合征难以治疗以及 Zucker 肥胖大鼠进食行为改变的原因。
