Inoue S, Satoh S, Tanaka K, Takamura Y, Murase T
Third Department of Internal Medicine, Yokohama City University, Japan.
Am J Physiol. 1993 Oct;265(4 Pt 2):R786-91. doi: 10.1152/ajpregu.1993.265.4.R786.
The present study investigated the mechanism of fasting hypertriglyceridemia in ventromedial hypothalamic (VMH) obesity by measurement of post-heparin plasma lipoprotein lipase (LPL) activity, triglyceride secretion rate (TGSR), and plasma insulin. One week after VMH lesions, when the lesioned rats were gaining weight rapidly (the dynamic phase), they showed normal plasma triglyceride levels with increased plasma LPL activity and TGSR. There was a positive correlation between hyperinsulinemia and elevated plasma LPL activity or TGSR in VMH-lesioned rats, while no correlation was observed in control rats. Ten weeks after VMH lesions, when the rats had become obese and reached a steady-state weight gain (the static phase), they showed hypertriglyceridemia with increased plasma LPL activity and TGSR. There was, again, a positive correlation between hyperinsulinemia and elevated plasma LPL activity or TGSR in VMH-lesioned rats. These results suggest a possible mechanism of fasting hypertriglyceridemia in these rats; in the dynamic phase adipose tissue adequately takes up circulating triglyceride because the tissue has sufficient take-up capacity and hence hypertriglyceridemia does not develop. In the static phase the tissue cannot adequately take up circulating triglyceride because of a limitation of its capacity, resulting in hypertriglycemia despite enhanced triglyceride secretion and increased LPL activity in both phases.
本研究通过测量肝素后血浆脂蛋白脂肪酶（LPL）活性、甘油三酯分泌率（TGSR）和血浆胰岛素，探讨腹内侧下丘脑（VMH）肥胖大鼠空腹高甘油三酯血症的机制。VMH损伤一周后，当损伤大鼠体重迅速增加时（动态期），它们的血浆甘油三酯水平正常，但血浆LPL活性和TGSR升高。VMH损伤大鼠的高胰岛素血症与血浆LPL活性或TGSR升高之间存在正相关，而对照组大鼠未观察到相关性。VMH损伤10周后，当大鼠变得肥胖并达到体重增加的稳定状态时（静态期），它们出现高甘油三酯血症，同时血浆LPL活性和TGSR升高。VMH损伤大鼠的高胰岛素血症与血浆LPL活性或TGSR升高之间再次存在正相关。这些结果提示了这些大鼠空腹高甘油三酯血症的一种可能机制；在动态期，脂肪组织能够充分摄取循环中的甘油三酯，因为该组织具有足够的摄取能力，因此不会发生高甘油三酯血症。在静态期，由于其能力的限制，该组织不能充分摄取循环中的甘油三酯，尽管在两个阶段甘油三酯分泌增加且LPL活性增强，但仍导致高甘油三酯血症。
