Chen Y D, Howard J, Huang V, Kraemer F B, Reaven G M
Diabetes. 1980 Aug;29(8):643-7. doi: 10.2337/diab.29.8.643.
Insulin deficiency was produced by streptozotocin in young (5-6 wk old) male rats, and measurements were made of plasma triglyceride and glucose concentrations and of lipoprotein lipase (LPL) activity of adipose tissue (epididymal) and muscle (gastrocnemius and soleus). Rats with streptozotocin-induced diabetes underwent a significant reduction in adipose tissue LPL activity (both total and heparin releasable), but the fall in LPL activity in these rats bore little relationship to their rise in plasma triglyceride concentration. Furthermore, muscle LPL activity was essentially unchanged in diabetic rats. Qualitatively similar changes were observed when measurements were made at either 8 a.m. (after the normal evening access to food) or 2 p.m. (6 h after food withdrawal). It is concluded that the hypertriglyceridemia that occurs secondary to insulin deficiency is not a simple function of decreased tissue LPL activity.
用链脲佐菌素诱导年轻(5 - 6周龄)雄性大鼠产生胰岛素缺乏,然后测定血浆甘油三酯和葡萄糖浓度以及脂肪组织(附睾)和肌肉(腓肠肌和比目鱼肌)的脂蛋白脂肪酶(LPL)活性。链脲佐菌素诱导的糖尿病大鼠的脂肪组织LPL活性(总活性和肝素可释放活性)显著降低,但这些大鼠LPL活性的下降与其血浆甘油三酯浓度的升高关系不大。此外,糖尿病大鼠的肌肉LPL活性基本未变。无论是在上午8点(正常夜间进食后)还是下午2点(禁食6小时后)进行测量,都观察到了定性相似的变化。得出的结论是,继发于胰岛素缺乏的高甘油三酯血症并非组织LPL活性降低的简单结果。