Feingold K R, Grunfeld C
J Clin Invest. 1987 Jul;80(1):184-90. doi: 10.1172/JCI113046.
The hyperlipidemia accompanying infection has been attributed to production of tumor necrosis factor. This cytokine inhibits adipose tissue lipoprotein lipase, which could decrease clearance of lipoproteins. Infections also increase hepatic lipogenesis. We now have demonstrated that tumor necrosis factor-alpha stimulates lipid synthesis in vivo. 2 h after administration of tumor necrosis factor (25 micrograms/200 g), plasma triglycerides increase 2.2-fold and remain elevated for 17 h. Plasma cholesterol also increases, but this effect appears after 7 h. Tumor necrosis factor rapidly stimulates incorporation of tritiated water into fatty acids in the liver (1-2 h), which persists for 17 h. Also, tumor necrosis factor stimulates hepatic sterol synthesis. Of note, tumor necrosis factor treatment does not stimulate lipid synthesis in other tissues, including adipose tissue. Labeled fatty acids rapidly increase in the plasma, raising the possibility that stimulation of hepatic lipogenesis by tumor necrosis factor contributes to the hyperlipidemia of infection.
伴随感染出现的高脂血症被认为与肿瘤坏死因子的产生有关。这种细胞因子会抑制脂肪组织脂蛋白脂肪酶，进而可能降低脂蛋白的清除率。感染还会增加肝脏脂肪生成。我们现已证明，肿瘤坏死因子-α在体内可刺激脂质合成。给予肿瘤坏死因子（25微克/200克）2小时后，血浆甘油三酯增加2.2倍，并在17小时内持续升高。血浆胆固醇也会增加，但这种效应在7小时后才出现。肿瘤坏死因子能迅速刺激肝脏中氚水掺入脂肪酸（1 - 2小时），并持续17小时。此外，肿瘤坏死因子会刺激肝脏固醇合成。值得注意的是，肿瘤坏死因子处理不会刺激包括脂肪组织在内的其他组织的脂质合成。标记的脂肪酸在血浆中迅速增加，这增加了肿瘤坏死因子刺激肝脏脂肪生成导致感染性高脂血症的可能性。
