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Tumor Necrosis Factor Alpha Knockout Promotes Adipose Fatty Acid Oxidation and Attenuates Insulin Resistance and Hepatic Steatosis in High Fat Diet-Fed Mice

机译:肿瘤坏死因子α基因敲除促进高脂饮食喂养小鼠的脂肪脂肪酸氧化并减轻胰岛素抵抗和肝脂肪变性。

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摘要

Substantial evidence indicates that adipose tissue (AT) dysfunction and lipid spillover in obesity promote insulin resistance and non-alcoholic fatty liver disease. Tumor necrosis factor alpha (TNFα) is one of the pro-inflammatory cytokines overexpressed in obesity and its knockout (KO) attenuates diet-induced adiposity, lipid deposition in the liver and insulin resistance. However, the potential roles played by TNFα in fatty acid metabolism in AT have been incompletely understood. The objective of this study was to investigate the role of TNFα in obesity-induced insulin resistance with the goal of providing a potential target for therapeutics.
机译:大量证据表明,肥胖患者的脂肪组织(AT)功能障碍和脂质溢出会促进胰岛素抵抗和非酒精性脂肪肝疾病。肿瘤坏死因子α(TNFα)是肥胖症中过度表达的促炎细胞因子之一,其敲除(KO)可减轻饮食引起的肥胖,肝脏脂质沉积和胰岛素抵抗。然而,尚未完全了解TNFα在AT脂肪酸代谢中的潜在作用。这项研究的目的是研究TNFα在肥胖诱导的胰岛素抵抗中的作用,以期为治疗提供潜在的靶标。

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