Kaufmann R L, Matson C F, Beisel W R
J Infect Dis. 1976 May;133(5):548-55. doi: 10.1093/infdis/133.5.548.
The role of Salmonella typhimurium endotoxin in producing hypertriglyceridemia was investigated in 70 male rhesus monkeys. Dose-response studies were performed with 0.3-9.0 mg of endotoxin/kg injected intravenously; free fatty acids and triglycerides were measured during the subsequent 8 hr. The effect of endotoxin on lipid disposal mechanisms was assessed by both intravenous lipid-loading tests and total plasma lipolytic activity after administration of heparin. The possible interference of endotoxin with lipid-clearing enzymes was also explored. Smaller doses of endotoxin (0.3 and 0.9 mg/kg) produced significant increments in free fatty acids within 2-5 hr of administration, with minimal trilgyceride increments. Larger doses of endotoxin (2.8-9.0 mg/kg) failed to produce significant elevations in free fatty acids but did result in significant triglyceride increases 2-6 hr after administration. Within 4 hr after administration of 7 mg of endotoxin/kg, both tests showed impaired disposal of lipids. However, once lipid-clearing enzymes were activated, endotoxin did not reduce lipolytic activity in vitro. These results support the contention that endotoxin significantly elevates serum triglyceride concentrations and leads to impaired lipid disposal mechanisms by interfering with the activation of lipid-clearing enzymes.
在70只雄性恒河猴中研究了鼠伤寒沙门氏菌内毒素在产生高甘油三酯血症中的作用。静脉注射0.3 - 9.0毫克内毒素/千克进行剂量反应研究；在随后的8小时内测量游离脂肪酸和甘油三酯。通过静脉脂质负荷试验和给予肝素后的总血浆脂解活性评估内毒素对脂质代谢机制的影响。还探讨了内毒素对脂质清除酶的可能干扰。较小剂量的内毒素（0.3和0.9毫克/千克）在给药后2 - 5小时内使游离脂肪酸显著增加，甘油三酯增加 minimal。较大剂量的内毒素（2.8 - 9.0毫克/千克）未能使游离脂肪酸显著升高，但在给药后2 - 6小时确实导致甘油三酯显著增加。给予7毫克内毒素/千克后4小时内，两项试验均显示脂质代谢受损。然而，一旦脂质清除酶被激活，内毒素在体外并不会降低脂解活性。这些结果支持这样的观点，即内毒素通过干扰脂质清除酶的激活而显著提高血清甘油三酯浓度并导致脂质代谢机制受损。
