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首页> 外文期刊>The Journal of Nutritional Biochemistry >Role of tumor necrosis factor alpha (TNFalpha) in the onset of fructose-induced nonalcoholic fatty liver disease in mice.
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Role of tumor necrosis factor alpha (TNFalpha) in the onset of fructose-induced nonalcoholic fatty liver disease in mice.

机译：肿瘤坏死因子α（TNFalpha）在果糖诱导的小鼠非酒精性脂肪肝疾病发作中的作用。

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Tumor necrosis factor alpha (TNFalpha) is known to be involved in dysregulation of hepatic lipid metabolism and insulin signaling. However, whether TNFalpha also plays a casual role in the onset of fructose-induced nonalcoholic fatty liver disease (NAFLD) has not yet been determined. Therefore, wild-type and TNFalpha receptor 1 (TNFR1)-/- mice were fed with either 30% fructose solution or plain tap water. Hepatic triglycerides, markers of inflammation and ATP concentration as well as plasma ALT levels were determined. Hepatic PAI-1, SREBP-1, FAS mRNA expression was assessed by real-time RT-PCR. Furthermore, lipid peroxidation and indices of insulin resistance were determined in liver tissue and plasma. In comparison to water controls, chronic intake of 30% fructose solution caused a significant ~5-fold increase in triglyceride accumulation and neutrophil infiltration in livers of wild-type mice and a ~8-fold increase in plasma ALT levels. In TNFR1-/- mice, hepatic steatosis was attenuated and neutrophil infiltration in the liver as well as plasma ALT levels was similar to water controls. The protective effect of the TNFR1 deletion against the onset of fructose-induced steatosis was associated with increased phospho AMPK and Akt levels, decreased SREBP-1 and FAS expression in the liver and decreased RBP4 plasma levels, whereas hepatic lipid peroxidation, iNOS protein and ATP levels were similar between wild-type and TNFR1-/- mice fed fructose. Taken together, these data suggest that TNFalpha plays a casual role in the onset of fructose-induced liver damage as well as insulin resistance in mice through signaling cascades downstream of TNFR1. Copyright Copyright 2011 Elsevier Inc. All rights reserved.
机译：已知肿瘤坏死因子α（TNFalpha）参与肝脂质代谢和胰岛素信号传导的失调。然而，尚未确定TNFalpha在果糖诱导的非酒精性脂肪肝疾病（NAFLD）发作中是否也起偶然作用。因此，野生型和TNFalpha受体1（TNFR1）-/-小鼠饲喂30％果糖溶液或自来水。测定肝甘油三酸酯，炎症标志物和ATP浓度以及血浆ALT水平。通过实时RT-PCR评估肝PAI-1，SREBP-1，FAS mRNA表达。此外，在肝组织和血浆中测定脂质过氧化和胰岛素抵抗指数。与水控制相比，长期摄入30％果糖溶液会导致野生型小鼠肝脏中甘油三酸酯的积累和中性粒细胞浸润显着增加约5倍，血浆ALT水平则增加约8倍。在TNFR1-/-小鼠中，肝脂肪变性减弱，肝脏中的中性粒细胞浸润以及血浆ALT水平与水对照相似。 TNFR1缺失对果糖性脂肪变性发作的保护作用与磷酸化AMPK和Akt水平升高，肝脏SREBP-1和FAS表达降低以及RBP4血浆水平降低有关，而肝脂质过氧化，iNOS蛋白和ATP喂果糖的野生型和TNFR1-/-小鼠之间的水平相似。综上所述，这些数据表明，TNFα通过信号转导TNFR1的下游级联，在果糖诱导的肝损伤以及胰岛素抵抗中起着偶然的作用。版权版权所有2011 Elsevier Inc.保留所有权利。

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