Nomura T, Hagino Y, Gotoh M, Iguchi A, Sakamoto N
Lipids. 1984 Aug;19(8):594-9. doi: 10.1007/BF02534717.
Fasting in normal rats produced a fall in hepatic triglyceride lipase (H-TGL) activity as well as lipoprotein lipase (LPL) activities of adipose tissue and psoas minor muscle. On the other hand, LPL activities of heart and diaphragm were not decreased by fasting; the former, in fact, was increased significantly. Changes in tissue specific lipase activity caused by withdrawal of insulin from insulin-treated diabetic animals paralleled in direction the changes induced by starvation of normal rats. Furthermore, it was shown in the present paper that the tissue specific lipase activity of diabetic rats became stuck in the starve phase of the starve-feed cycle regardless of dietary intake. The changes of the tissue specific lipase activities, especially of liver, adipose tissue and heart, appeared to coincide with those of plasma insulin levels. These results strongly suggest that the tissue specific lipase system is under hormonal regulation by insulin. Streptozotocin diabetes produced hypertriglyceridemia. The possible mechanism of the hypertriglyceridemia in diabetic animals was discussed in connection with the role of the tissue specific lipase system in the serum triglyceride metabolism.
正常大鼠禁食会导致肝脏甘油三酯脂肪酶(H-TGL)活性以及脂肪组织和腰小肌脂蛋白脂肪酶(LPL)活性下降。另一方面,心脏和膈肌的LPL活性不会因禁食而降低;事实上,前者会显著增加。胰岛素治疗的糖尿病动物停止使用胰岛素后,组织特异性脂肪酶活性的变化方向与正常大鼠饥饿诱导的变化相似。此外,本文表明,糖尿病大鼠的组织特异性脂肪酶活性无论饮食摄入情况如何,都会停留在饥饿-进食周期的饥饿阶段。组织特异性脂肪酶活性的变化,尤其是肝脏、脂肪组织和心脏的变化,似乎与血浆胰岛素水平的变化一致。这些结果有力地表明,组织特异性脂肪酶系统受胰岛素的激素调节。链脲佐菌素诱导的糖尿病会导致高甘油三酯血症。结合组织特异性脂肪酶系统在血清甘油三酯代谢中的作用,讨论了糖尿病动物高甘油三酯血症的可能机制。