TUMOR-NECROSIS-FACTOR-ALPHA STIMULATES HEPATIC LIPOGENESIS IN THE RAT INVIVO
TUMOR-NECROSIS-FACTOR-ALPHA STIMULATES HEPATIC LIPOGENESIS IN THE RAT INVIVO
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DOI：
10.1172/jci113046
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发表时间：
1987-07-01
影响因子：
15.9
通讯作者：
GRUNFELD, C
中科院分区：
文献类型：
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作者：
FEINGOLD, KR;GRUNFELD, C
伴随感染的高脂血症与肿瘤坏死因子的产生有关。该细胞因子抑制脂肪组织脂蛋白脂肪酶，可降低脂蛋白清除率。感染也会增加肝脏脂肪生成。我们现在已经证明肿瘤坏死因子- α刺激体内脂质合成。肿瘤坏死因子（25 .mu）给药后2 h。g/200 g)，血浆甘油三酯增加2.2倍，并持续升高17小时。血浆胆固醇也增加，但这种作用在7小时后才出现。肿瘤坏死因子迅速刺激氚化水与肝脏脂肪酸结合（1-2小时），持续17小时。此外，肿瘤坏死因子刺激肝脏固醇合成。值得注意的是，肿瘤坏死因子治疗不会刺激其他组织（包括脂肪组织）的脂质合成。血浆中标记脂肪酸迅速增加，提高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。
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 .mu.g/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 persistsfor 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.