Rosato E F, Vemulapalli P, Lang C H, Lanza-Jacoby S
Department of Surgery, Jefferson Medical College of Thomas Jefferson University, Philadelphia, Pennsylvania 19107, USA.
J Surg Res. 1997 Nov;73(1):73-9. doi: 10.1006/jsre.1997.5199.
Gram-negative sepsis suppresses lipoprotein lipase (LPL) activity in adipose tissue which contributes, in part, to the altered clearance of triglycerides. The suppression in LPL activity occurs when plasma insulin concentrations are elevated and insulin-stimulated glucose utilization is impaired. This study was planned to evaluate whether the presence of insulin resistance was responsible for the decrease in adipose LPL activity. Adipocytes were isolated from epididymal fat pads 24 h after inducing sepsis in male Lewis rats by intravenous injection of 4 x 10(8) colonies of live Escherichia coli/100 g body wt. The decrease in heparin-releasable (HR) LPL activity in adipocytes from the septic rats was evident at the time of isolation and maintained in a 20-h culture. After overnight incubation with insulin (10(-8) M), HR LPL activity was stimulated to a greater extent in adipocytes from septic rats (298%) than in adipocytes from control rats (88%). The insulin stimulation of LPL activity during sepsis could not be attributed to insulin-like growth factor-I (IGF-I) as adipocytes from septic rats appeared to be IGF-I resistant. Insulin-treatment (10(-8) M) increased LPL synthesis 99% in adipocytes from control rats and 136% in adipocytes from septic rats. Insulin treatment also led to a 65 and 62% increase in LPL mass in adipocytes from control and septic rats, respectively. These findings indicate that the sepsis-induced decrease in adipose LPL is not due to insulin resistance with respect to LPL. The insulin stimulation of LPL activity in adipocytes from septic rats appears to be mediated by an increase in LPL synthesis.
革兰氏阴性菌败血症会抑制脂肪组织中的脂蛋白脂肪酶（LPL）活性，这在一定程度上导致了甘油三酯清除率的改变。当血浆胰岛素浓度升高且胰岛素刺激的葡萄糖利用受损时，LPL活性就会受到抑制。本研究旨在评估胰岛素抵抗的存在是否是脂肪组织LPL活性降低的原因。通过静脉注射4×10⁸个活大肠杆菌菌落/100克体重，在雄性Lewis大鼠中诱导败血症24小时后，从附睾脂肪垫中分离脂肪细胞。败血症大鼠脂肪细胞中肝素可释放（HR）LPL活性的降低在分离时就很明显，并在20小时的培养中保持。在与胰岛素（10⁻⁸ M）过夜孵育后，败血症大鼠脂肪细胞中HR LPL活性的刺激程度（298%）比对照大鼠脂肪细胞（88%）更大。败血症期间胰岛素对LPL活性的刺激不能归因于胰岛素样生长因子-I（IGF-I），因为败血症大鼠的脂肪细胞似乎对IGF-I有抗性。胰岛素处理（10⁻⁸ M）使对照大鼠脂肪细胞中的LPL合成增加99%，使败血症大鼠脂肪细胞中的LPL合成增加136%。胰岛素处理还分别使对照大鼠和败血症大鼠脂肪细胞中的LPL质量增加了65%和62%。这些发现表明，败血症诱导的脂肪组织LPL降低并非由于对LPL的胰岛素抵抗。败血症大鼠脂肪细胞中胰岛素对LPL活性的刺激似乎是由LPL合成增加介导的。
