Liu L, Severson D L
Medical Research Council Signal Transduction Group, Faculty of Medicine, University of Calgary, Canada.
Can J Physiol Pharmacol. 1995 Mar;73(3):369-77. doi: 10.1139/y95-047.
The decrease in myocardial lipoprotein lipase (LPL) activity observed previously in acute, severe models of insulin-deficient diabetes may be a compensatory response to hypertriglyceridemia and a sustained increase in fatty acid delivery to cardiomyocytes. The administration of fructose (10% solution in the drinking water for 4 days) to rats produced hypertriglyceridemia, but heparin-releasable LPL activity from perfused hearts and total and heparin-releasable LPL activities in isolated cardiomyocytes were not reduced. The acute (4 day) induction of a mild diabetic state (60 mg/kg streptozotocin) resulted in modest hypertriglyceridemia, and a selective decrease in heparin-releasable LPL activity in perfused hearts; LPL activity in cardiomyocytes from diabetic rat hearts was not reduced. Therefore, the diabetes-induced fall in myocardial LPL activity is not secondary to hypertriglyceridemia, since fructose treatment did not change LPL activity. Perfusion of rat hearts with 100 microM lysophosphatidylcholine (LPC) released a small amount of LPL activity into the perfusate, but only if albumin was omitted from the perfusion solution. Thus, the selective reduction in heparin-releasable LPL activity in perfused diabetic hearts is probably not the consequence of displacement by LPC, a lipolytic product of the LPL-catalyzed degradation of triacylglycerol-rich lipoproteins. Circulating LPL activity in the plasma of diabetic rats was not decreased relative to control plasma enzyme activity; therefore, the reduction in heparin-releasable LPL activity is not because circulating LPL was less available for uptake by the endothelium in diabetic hearts.
先前在胰岛素缺乏型糖尿病的急性严重模型中观察到的心肌脂蛋白脂肪酶（LPL）活性降低，可能是对高甘油三酯血症以及向心肌细胞脂肪酸输送持续增加的一种代偿反应。给大鼠饮用含10%果糖的溶液4天可导致高甘油三酯血症，但灌注心脏中肝素可释放的LPL活性以及分离的心肌细胞中的总LPL活性和肝素可释放的LPL活性并未降低。急性（4天）诱导轻度糖尿病状态（60mg/kg链脲佐菌素）导致中度高甘油三酯血症，以及灌注心脏中肝素可释放的LPL活性选择性降低；糖尿病大鼠心脏的心肌细胞中的LPL活性未降低。因此，糖尿病诱导的心肌LPL活性下降并非继发于高甘油三酯血症，因为果糖处理并未改变LPL活性。用100μM溶血磷脂酰胆碱（LPC）灌注大鼠心脏会向灌注液中释放少量LPL活性，但前提是灌注溶液中不含白蛋白。因此，灌注的糖尿病心脏中肝素可释放的LPL活性选择性降低可能不是LPC置换的结果，LPC是LPL催化富含三酰甘油的脂蛋白降解的脂解产物。与对照血浆酶活性相比，糖尿病大鼠血浆中的循环LPL活性并未降低；因此，肝素可释放的LPL活性降低并非因为循环LPL在糖尿病心脏中被内皮摄取的可用性降低。
